STANDARD TREATMENT GUIDELINES

Diseases of the Ear Nose and Throat (ENT)

DEPARTMENT OF HEALTH AND FAMILY WELFARE GOVERNMENT OF KERALA

STANDARD TREATMENT GUIDELINES IN ENT Four sections Section I Common diseases of EAR Section II Common diseases of Nose Section III Common diseases of Throat Section IV ENT emergencies

Committee for development of Standard Treatment guidelines ENT CONVENOR Dr. Suchit Roy B R Professor & HOD of ENT, Government Medical College, Thrissur MEMBERS Dr. Satheesh S, Professor & HOD of ENT, GMC, Thiruvananthapuram Dr. Sunil Kumar K P, Professor of ENT, GMC, Kozhikode Dr. Venugopal M, Professor, GMC, Thiruvananthapuram Dr. Shibu George, Professor & HOD of ENT, GMC, Kottayam Dr. Sadarudheen Ahmed, Professor & HOD, GMC Eranakulam Dr. Herman Guild M John, Professor & HOD, GMC Alappuzha Dr. Thulaseedharan S, Additional Professor & HOD, GMC, Kollam Dr. Suma Radhakrishnan, Additional Professor of ENT, GMC, Manjeri, Dr. Binu Raju George, Associate Professor, GMC, Thrissur Dr. Susan James, Associate Professor of ENT, GMC,Thiruvananthapuram Dr. Sindhu V Nath, Associate Professor of ENT, GMC, Thiruvananthapuram Dr. Salima Rema Windsor, Associate Professor of ENT, GMC, Kollam Dr. Divya G M, Assistant Professor of ENT, GMC, Kozhikode Dr. Salil Kumar K, Principal, SUT MC, Thiruvananthapuram Dr. Paul Samuel, Sr Consultant, Cosmopolitan Hospital, Thiruvananthapuram & Secretary, AOI, Thiruvananthapuram Chapter, Kerala State EXTERNAL EXPERT Dr. Rupa Vedantam, Professor & HOD, CMC Vellore

“Driven by the inspiration drawn from Shri. Rajeev Sadanandan IAS, Additional Chief Secretary, Department of Health and Family Welfare, Government of Kerala, the process of preparation of Standard Treatment Guidelines (STG) was initiated by the Director of Medical Education Dr. Remla Beevi A. The process of developing and finalizing the STG’s were coordinated by Dr. Sreekumari K. Joint Director Medical education and Dr. Suma T K, Professor of Medicine and ably supported by a dedicated team of experts, including external faculty”.

TABLE OF CONTENTS Message from CM 9 Message from HM 11 Foreword ACS 13 1. Common diseases of ear 15 1.1 Definition 17 1.2 Acute otitis externa 17 1.3 Malignant external otitis 20 1.4 Acute otitis media in children 24 1.5 Otitis media with effusion 29 1.6 Chronic otitis media 34 1.7 Permanent childhood hearing loss 38 1.8 Idiopathic sudden SNHL 42 1.9 Bell's palsy 45 1.10 Ménière's disease 49 1.11 Benign paroxysmal positional vertigo 51 2. Common diseases of nose 55 2.1 Rhinosinusitis 57 2.1.1 Introduction 57 2.1.2 Acute rhinosinusitis 57 2.1.3 Chronic rhinosinusitis in adults 59 2.1.4 Chronic rhinosinusitis in children 61 2.1.5 Fungal sinusitis 61 2.1.6 Fungal Rhinosinusitis 61 2.2 Epistaxis 68 2.3 Allergic rhinitis 74 3. Common diseases of throat 81 3.1 Cut throat 83 3.2 Dysphagia 91 3.3 Dysphonia 97 3.4 Foreign body throat 101 3.5 Deep neck space infections 104 3.6 Stridor 112 4. ENT emergencies 117 4.1 Facial trauma 119 4.2 Ear trauma 121 4.3 Facial paralysis 123 4.4 Ear ache 125 4.5 Foreign body ear 127 4.6 Foreign body nose 129 4.7 Headache 131 4.8 Vertigo 134 Message

Pinarayi Vijayan Secretariat Chief Minister Thiruvananthapuram

The Government is taking many initiatives to ensure providing quality health care to all. Out of the five missions launched by the Government, the Aardram mission is primarily focussed to improve Primary Health Care to provide standard health care facilities to people at grassroots. This initiative is complemented by strategic investment for the improvement of infrastructure in secondary and tertiary health care institutions to provide quality health care services. I am happy to note that the Department of Health is also taking initiatives to bring standardization in treatment for various disciplines like Cardiology, Critical care, Diabetes Mellitus, Cancer Care, etc. It is a noteworthy initiative to improve the qualitative aspects of the health service delivery. I appreciate the efforts taken by the experts from Government sector and private sector from Kerala and also the subject experts from outside the state. I am hopeful that the introduction of standard guidelines for diagnosis and treatment will ensure better quality and consistency in health care. I wish all the success to this endeavour.

Pinarayi Vijayan Chief Minister

9

Message

11

Foreword

Patient care has moved away from management by an individual based on personal knowledge and skill to an evidence based, team managed operation. Decisions are reviewed more rigorously post facto and their alignment verified with standard practice. With the mode of payment for care moving from out of pocket payments to third party payers there will be a demand for rigorous documentation and evidence of having conformed to standard practice. When analysis of big data and machine learning becomes the norm it will require a standard set of procedures to act as the baseline from which to measure deviations and differences in impact. To meet the requirement of these developments in the field of medicine, it is necessary to have explicit, objectively verifiable set of standard operating procedures. They have to be prepared based on international guidelines with the highest acceptance, but have to be modified to suit local knowledge and practice, so that there is local ownership. Government of Kerala has been trying to get the guidelines prepared for some time now. I would like to thank and congratulate Dr. Sreekumari, Joint Director of Medical Education and Dr. T.K.Suma, Professor of Medicine, T.D. Medical College, Alappuzha who took on the task of preparing standard treatment guidelines and completed it through a long, consultative process. I also thank the conveners of the different thematic groups who coordinated the work in their field as well as the innumerable number of participants, in government and private sector, who contributed their effort and knowledge to improve the guidelines. Professional associations have also contributed in their fields. Their efforts have resulted in a product they and Kerala can be proud of. Treatment guidelines cannot be static if they are to remain relevant. They must be updated based on new knowledge and the

13 experience of treatment based on these guidelines. To do this the group which prepared the guidelines has to remain active and have a system for collecting data on the results of practice based on these guidelines. I hope such an activity is institutionalised and periodic revisions of the guidelines are prepared and published.

I wish that these guidelines contribute to raising the quality of patient care in Kerala.

Rajeev Sadanandan IAS Addl Chief Secretary Health & Family Welfare Department

14 Section I Common diseases of EAR

STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section I

Section I 1. COMMON DISEASES OF THE EAR SCOPE The purpose of this guidelines is to identify quality improvement opportunities in managing common diseases of the ear and to create explicit recommendations to implement these opportunities in clinical practice. Specifically, it is intended to educate all specialists involved in the evidence-based management of ear diseases with set goals to improve diagnostic accuracy, identify sequelae or complications early, advice rational investigations and prescribe only scientific treatment. This guideline is applicable in any setting where patients with ear disease would be identified, monitored, or managed. This guidelines, however, does not apply to management of ear diseases at the primary care set up. 1.1 DEFINITION The management guidelines of common ear diseases comprises of guidelines for diagnosis of ear diseases based on symptoms and signs, essential investigations to confirm the diagnosis and rational treatment options, both medical and surgical. PURPOSE OF RECORD To ensure uniform, scientific and ethical management of common ear disease 1.2 ACUTE OTITIS EXTERNA INTRODUCTION Defined as diffuse or localized inflammation of the external ear canal, which may also involve the pinna or tympanic membrane. Usually represents acute bacterial infection of the external canal (most commonly Pseudomonas aeruginosa & Staphylococcus aureus), but may also be caused by fungal infection, viruses or skin diseases. Key points in diagnosis ü Rapid onset; usually within 48 hours. ü H/O preceding trauma (e.g.; forceful ear cleaning, use of ear buds) OR exposure to water (e.g.: swimming) ü Symptoms: Earache (often severe) &/or jaw pain, itching, hearing loss or fullness, discharge. (Pain aggravated by jaw movements). ü Signs: Tenderness of the tragus, pinna, or both. ü Diffuse oedema of ear canal oedema, erythema, or both.

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ü Serous or purulent otorrhea, Pre / post aural lymphadenitis, Congested tympanic membrane. ü Sometimes presents as localized inflammation of hair follicle of cartilaginous canal (furunculosis); can lead to abscess formation. ü If otomycosis- thick greyish discharge with black (Aspergillus Niger) or white (Candida albicans) fungal colonies visualized on otoscopy (resemble wet news-paper when taken out). ü Routinely no investigations necessary. ü Culture & Sensitivity of the discharge recommended if immunocompromised; in adults with recurrent external otitis investigate to rule out latent Diabetes mellitus. MANAGEMENT GUIDELINES 1. Analgesics recommended based on the severity of pain. 2. Systemic antibiotics not recommended routinely for primary treatment, or uncomplicated external otitis. However, to be decided depending on disease severity and associated co-morbidities on presentation. 3. Extended indications for systemic antibiotics in acute otitis externa a) Extension outside the ear canal causing peri-aural cellulitis b) Presence of specific host factors that can modify disease like diabetes mellitus. 4. Topical preparations should be prescribed for initial therapy of uncomplicated external otitis. These include antibiotic (e.g.: Ciprofloxacin / Ofloxacin) + steroid ear drops & 1% Acetic acid irrigations Avoid ototoxic ear drops in presence of perforated tympanic membrane or grommet. Topical ear drops may also be avoided if tympanic membrane is not visible or if there is known history of allergy to the drug. 5. Do meticulous aural toilet to remove pus & fungal debris combined with ear packing (antibiotic + steroid cream / Ichthammol glycerin) when the ear canal is obstructed to facilitate topical drug delivery. 6. If refractory to initial therapy for 48-72 hours, review diagnosis & rule out other causes. 7. Specific advise to prevent recurrence should be given to patients like avoidance of probing the ear canal (e.g.: ear buds) and observing appropriate water precautions for the ear.

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Treatment Algorithm for External Otitis

REFERENCES 1. Rosenfeld RM, Brown L, Cannon CR, et al. Clinical practice guideline: acute otitis externa. Otolaryngol Head Neck Surgery. 2006; 134 (4 suppl): S4-S23. 2. Rosenfeld RM, Schwartz SR, Cannon CR, et al. Clinical practice guideline: acute otitis externa. Otolaryngol Head Neck Surg. 2014 Feb; 150(1 Suppl): S1-S24 3. Ruckenstein MJ. Infections of the external ear. In: Cummings Otolaryngology: Head & Neck Surgery. 4th ed. Philadelphia, PA: Mosby; 2005:2979-2987. 4. Rosenfeld RM, Singer M, Wasserman JM, Stinnett SS. Systematic review of topical antimicrobial therapy for acute otitis externa. Otolaryngol Head Neck Surg. 2006;134(4 suppl):S24-48. 5. Nussinovitch M, Rimon A, Volovitz B, Raveh E, Prais D, Amir J. Cotton- tip applicators as a leading cause of otitis externa. Int J Pediatr Otorhinolaryngol. 2004;68(4):433-435. 6. Sander R. Otitis externa: a practical guide to treatment and prevention. Am Fam Physician. 2001;63(5):927-936, 941-922. 7. Burton MJ, Singer M, Rosenfeld RM. Extracts from The Cochrane Library:

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interventions for acute otitis externa. Otolaryngol Head Neck Surg. 2010;143(1):8-11. 8. Pond F, McCarty D, O'Leary S. Randomized trial on the treatment of edematous acute otitis externa using ear wicks or ribbon gauze: clinical outcome and cost. J Laryngol Otol. 2002;116(6):415-419. 9. Rutka J. Acute otitis externa: treatment perspectives. Ear Nose Throat J. 2004;83(9 suppl 4):20-21. 10. Van Balen FA, Smit WM, Zuithoff NP, Verheij TJ. Clinical efficacy of three common treatments in acute otitis externa in primary care: randomized controlled trial. BMJ. 2003;327(7425):1201-1205. 1.3 MALIGNANT OTITIS EXTERNA INTRODUCTION Malignant (Necrotizing) external otitis is a highly fatal invasive infection of the external auditory canal and temporal bone which is usually seen in elderly diabetics and immunocompromised individuals. The infection begins as external otitis but rapidly spreading cellulitis along the facial planes of bony canal can lead to osteomyelitis of the temporal bone and skull base. Unchecked patient may develop multiple cranial nerve palsy, intracranial suppuration and even death. Most common organism implicated is Pseudomonas aeruginosa, though other microbials like Staphylococci, Proteus mirabilis, Klebsiella species and Aspergillus fumigatus have been described. Criteria for diagnosis (Presence 3 or more) 1. Refractory otitis externa 2. Severe nocturnal otalgia 3. Purulent otorrhea 4. Granulation tissue deep canal, especially osseocartilaginous junction 5. Growth of Pseudomonas aeruginosa in culture 6. Presence of diabetes or any other immunocompromised state Apart from the diagnostic criteria points of importance to be noted in diagnosis of malignant otitis externa: a) Inflammatory changes may spread to peri-aural tissue; deep tenderness may be elicited at the soft tissue between the ramus of mandible and mastoid tip. b) Tympanic membrane usually appears normal (if visualized).

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c) Persistent temporal headaches, altered mentation, diplopia, hoarseness, dysphagia & facial asymmetry may signify onset of complications like intracranial spread and cranial nerve palsies d) Most common cranial nerve involved is facial; but any nerve between V- XII may be affected) e) Other immunocompromised states apart from diabetes to be kept in mind including renal failure, transplant recipients, disseminated malignancies, anti-malignancy chemotherapy, lymphoproliferative disorders and AIDS. MANAGEMENT Investigations ü Do preliminary ESR / CRP as aids to monitor disease progression ü Take an ear swab for culture & sensitivity right at first visit, before initiating antibiotic therapy to direct future change in antibiotic therapy if needed ü HRCT temporal bone & skull should be the primary radiological investigation to assess extent of disease and complications; however, CT may fail to diagnose early skull base osteomyelitis Supportive investigations (Not mandatory) ü MRI evaluation is mainly indicated to supplement HRCT in special situations like suspected intra-cranial complications. ü When available Technetium (Tc99) & Gallium (Ga67) bone scintigraphy should be undertaken to evaluate status of skull base osteomyelitis. ü Technetium scan is useful in the initial evaluation since a positive uptake confirms the diagnosis of skull base osteomyelitis. Gallium scan ü (Negative Ga uptake) may be used monitor disease resolution and is hence may be used as a prognostic marker. ü Granulation tissue if present should be obtained for biopsy to rule out malignancy of middle ear or external canal which masqueraded as MEO. ü In refractory, culture-negative malignant external otitis, a fungal cause should be suspected; a polymerase chain reaction (PCR) assay or biopsy may be useful.

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TREATMENT - MEDICAL CARE Antibiotics 1. Initial outpatient therapy may be started with oral Ciprofloxacin (750mg BID) in patients who do not require hospital admission for diabetes or pain management. [Ciprofloxacin should not be prescribed for patients with fluoroquinolone allergy, history of seizure disorder, cranial neuropathy or intracranial complications]. 2. Hospitalized patients should be started on intravenous ceftazidime which as monotherapy is the drug of choice. 3. Antibiotic therapy may also be changed as directed by the sensitivity pattern of the initial culture swab obtained 4. The duration of antibiotic therapy should be prolonged (at least 6-8 weeks) 5. Reduction in pain within 48 hours of starting therapy may be taken as the sign of sufficient therapeutic response; ESR/ CRP estimation may be used to monitor the disease progression. 6. Gallium scintigraphy (if available) may be used to decide duration of antibiotic therapy. Antibiotic may be stopped 1 week after Gallium scan returns to normal. 7. If treatment response is poor, consider modification of antibiotic therapy based on antibiogram or results of culture. Rule our fungal MEO in such cases; obtain deeper biopsies from ear Adjuvant therapy 1. Ototopic antimicrobial therapy may be initiated; preferably Ciprofloxacin/ Ofloxacin + Dexamethasone. Irrigation with 1% acetic acid solution should supplement topical antimicrobials 2. Aural toilet - Suction clearance of the discharge, removal of granulations followed by packing of the canal with antibiotic steroid cream may contribute to bringing down local inflammation 3. Meticulous glycemic control should be maintained; change over to insulin (if on OHA), Appropriate consultation with general physician / endocrinologist need be initiated 4. Manage any condition other than diabetes predisposing to MEO appropriately 5. Hyperbaric oxygen if available may be used as adjunctive therapy for patients with complications, experiencing a poor response to therapy, or with

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recurrent cases. 6. Surgery is reserved for local debridement, removal of bony sequestrum, and drainage of abscess (if any). Prognosis Prognostic factors in malignant external otitis include the duration of diabetes mellitus, the C-reactive protein level and the erythrocyte sedimentation rate. (inflammatory markers), the extent of the malignant external otitis as assessed through imaging studies, and cranial nerve involvement. Treatment Algorithm for Malignant External Otitis

REFERENCES 1. Karaman E, Yilmaz M, Ibrahimov M, Haciyev Y, Enver O. Malignant otitis externa. J Craniofac Surg. 2012 Nov. 23(6):1748-51. 2. Chandler JR. Malignant external otitis. Laryngoscope. 1968 Aug. 78(8):1257-94. 3. Phillips JS, Jones SE. Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa. Cochrane Database Syst Rev. 2013 May 31. 5:CD004617. 4. Chandler JR. Malignant external otitis: further considerations. Ann Otol Rhinol Laryngol. 1977 Jul-Aug. 86(4 Pt 1):417-28. 5. Franco-Vidal V, Blanchet H, Bebear C, Dutronc H, Darrouzet V. Necrotizing external otitis: a report of 46 cases. Otol Neurotol. 2007 Sep. 28(6):771-3. 6. Soudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of

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malignant external otitis with facial paralysis. Arch Otolaryngol Head Neck Surg. 2007 Oct. 133(10):1002-4. 7. Mani N, Sudhoff H, Rajagopal S, Moffat D, Axon PR. Cranial nerve involvement in malignant external otitis: implications for clinical outcome. Laryngoscope. 2007 May. 117(5):907-10. 8. Nawas MT, Daruwalla VJ, Spirer D, Micco AG, Nemeth AJ. Complicated necrotizing otitis externa. Am J Otolaryngol. 2013 Nov-Dec. 34(6):706- 9. 9. Sylvester MJ, Sanghvi S, Patel VM, Eloy JA, Ying YM. Malignant otitis externa hospitalizations: Analysis of patient characteristics. Laryngoscope. 2017 Oct. 127 (10):2328-36. 10. Hobson CE, Moy JD, Byers KE, et al. Malignant otitis externa: evolving pathogens and implications for diagnosis and treatment. Otolaryngol Head Neck Surg. 2014 Mar 26. 11. Gruber M, Roitman A, Doweck I, et al. Clinical utility of a polymerase chain reaction assay in culture-negative necrotizing otitis externa. Otol Neurotol. 2015 Apr. 36 (4):733-6. 12. Berenholz L, Katzenell U, Harell M. Evolving resistant pseudomonas to ciprofloxacin in malignant otitis externa. Laryngoscope. 2002 Sep. 112(9):1619-22. 13. Carlton DA, Perez EE, Smouha EE. Malignant external otitis: The shifting treatment paradigm. Am J Otolaryngol. 2018 Jan - Feb. 39 (1):41-5. 14. Lee SK, Lee SA, Seon SW, et al. Analysis of Prognostic Factors in Malignant External Otitis. Clin Exp Otorhinolaryngol. 2017 Sep. 10 (3):228-35. 1.4 ACUTE OTITIS MEDIA IN CHILDREN INTRODUCTION AOM is the rapid onset of signs and symptoms of inflammation in the middle ear cleft. It is predominantly a disease of childhood. History History varies with age; constant features in different age groups are as follows ü Neonates & infants: Irritability, excessive crying, ear tugging, lack of appetite or feeding difficulties. ü Children: Fever and otalgia; there may be associated vomiting. ü Older children & adults: Hearing loss, earache or ear stuffiness. ü Prior upper respiratory catarrh, nocturnal peak of otalgia followed by

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otorrhea may be common to all. ü Otorrhea is usually mucopurulent and may herald the onset of pain relief. Diagnosis Otoscopy is the gold standard. Look for ü Congestion and signs of inflammation on the tympanic membrane ü Later may appear cloudy & bulging. ü Small perforation may develop on the tympanic membrane ü Exudate seen oozing through the perforation; may be pulsatile Investigations Routinely not needed. MANAGEMENT 1. AOM management should include pain evaluation & appropriate management 2. Indications for antibiotics in AOM: a) AOM (Bilateral or unilateral) in children aged 6 months or above with severe signs / symptoms b) Bilateral AOM in Children aged 6-23 months even without severe signs / symptoms c) AOM in children aged < 6 months d) AOM with otorrhea in children Note ü Severe signs / symptoms - Moderate or severe otalgia, Otalgia ≥ 48 hours, Temperature ≥ 39°C ü Unilateral, non-severe AOM in children aged 6-23 months or all non- severe AOM in older children may be managed either with antibiotics OR observation & close follow-up. ü The decision not to give initial antibiotic treatment and observe should be a joint decision of the clinician and parents. In such cases, a system for close follow-up & starting antibiotics if symptoms worsen or no improvement is seen in 48 to 72 hours must be adapted. ü In children < 6 months even a presumptive diagnosis of AOM should receive antibiotics due to the higher prevalence of suppurative complications in this age group ü Children whose symptoms have worsened or not responded to the initial antibiotic treatment within 48-72 hours should be re-evaluated and

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treatment changed if indicated (Follow up mandatory) 3. Antibiotic policy in AOM: a) First line treatment: High dose Amoxicillin (80-90 mg/kg/day) is the antibiotic of choice unless the child received it within 30 days, has concurrent purulent conjunctivitis, or is allergic to penicillin; in these cases, clinicians should prescribe an antibiotic with additional beta- lactamase coverage. b) Duration: For children younger than 2 years and children with severe symptoms, a standard 10-day course is recommended. A seven day course of oral antibiotic is equally effective in children 2 to 5 years of age with mild or moderate AOM. For children 6 years and older with mild to moderate symptoms, a 5- to 7-day course is adequate. c) Second line antibiotics recommended are as follows: i. High-dose oral Amoxycillin-clavulanate (80-90 mg/kg/day of Amoxycillin component + 6.4 mg/kg/day of clavulanate component in two divided doses) ii. Oral Cefuroxime axetil (suspension, 30 mg/kg/day; tablet, 250 mg twice daily) iii. Intramuscular (IM) Ceftriaxone (administered as a single IM injection of 50 mg/kg on 3 consecutive days) iv. For children who are allergic to penicillin start 2nd/ 3rd generation Cephalosporins (Cefdinir, Cefuroxime, Cefpodoxime, Ceftriaxone) OR Macrolides (Azithromycin/ Clarithromycin) v. Tympanocentesis and culture of middle ear fluid should be considered for bacteriologic diagnosis and susceptibility testing when a series of antibiotic drugs have failed to improve the clinical condition. The other option to obtain information on the middle ear pathogens and their antimicrobial susceptibility is to obtain a nasopharyngeal specimen for bacterial culture 4. Indications for Myringotomy in AOM: a) Failed antimicrobial treatment with signs of local or systemic sepsis b) Complications requiring culture for adequate therapy c) Children who are immuno-suppressed or immunocompromised d) Neonates with AOM (more likely to have an unusual / invasive pathogen)

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5. Recurrent AOM More than 3 episodes in 6 months or 4 or more episodes in 1 year a) In children with recurrent AOM ventilation tube insertion is recommended to reduce the frequency of AOM episodes b) Ventilation tube insertion is not recommended in children with recurrent AOM who do not have middle ear effusion in either ear at the time of assessment. c) Adenoidectomy may be beneficial when performed along with placement of ventilation tubes or in children with previous tympanostomy tube placement. 6. Other recommendations a) Pneumococcal conjugate vaccination is recommended in all children b) Exclusive breastfeeding is recommended for 6 months or longer c) Eliminating exposure to passive tobacco smoke has been postulated to reduce the incidence of AOM in infancy. d) Avoiding supine bottle feeding (“bottle propping”) and reducing or eliminating pacifier use in the second 6 months of life may reduce AOM incidence.

Treatment Algorithm for AOM in children

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REFERENCES 1. Rettig E, Tunkel DE. Contemporary concepts in management of acute otitis media in children. Otolaryngol Clin North Am. 2014 Oct. 47 (5):651-72. 2. Minovi A, Dazert S. Diseases of the middle ear in childhood. GMS Curr Top Otorhinolaryngol Head Neck Surg. 2014. 13: Doc11. 3. Arola M, Ruuskanen O, Ziegler T, et al. Clinical role of respiratory virus infection in acute otitis media. Pediatrics. 1990 Dec. 86(6):848-55. 4. Block SL. Causative pathogens, antibiotic resistance and therapeutic considerations in acute otitis media. Pediatr Infect Dis J. 1997 Apr. 16(4):449-56. 5. Marchisio P, Esposito S, Picca M, et al. Prospective evaluation of the aetiology of acute otitis media with spontaneous tympanic membrane perforation. Clin Microbiol Infect. 2017 Jan 19. 6. Thomas JP, Berner R, Zahnert T, et al. Acute otitis media-a structured approach. Dtsch Arztebl Int. 2014 Feb 28. 111(9):151-60. 7. Boggs W. Antimicrobial Treatment of Acute Otitis Media Shortens Duration of Middle Ear Effusion. Medscape. May 9 2014. 8. Tapiainen T, Kujala T, Renko M, et al. Effect of Antimicrobial Treatment of Acute Otitis Media on the Daily Disappearance of Middle Ear Effusion: A Placebo-Controlled Trial. JAMA Pediatr. 2014 May 5. 9. Conrad DE, Levi JR, Theroux ZA, et al. Risk Factors Associated With Postoperative Tympanostomy Tube Obstruction. JAMA Otolaryngol Head Neck Surg. 2014 Jul 10. 10. Hasegawa J, Mori M, Showa S, et al. Pneumococcal vaccination reduced the risk of acute otitis media: a cohort study. Pediatr Int. 2015 Jan 23. 11. Tawfik KO, Ishman SL, Altaye M, Meinzen-Derr J, Choo DI. Pediatric Acute Otitis Media in the Era of Pneumococcal Vaccination. Otolaryngol Head Neck Surg. 2017 Mar 1. 194599817699599. 12. Kaur R, Morris M, Pichichero ME. Epidemiology of Acute Otitis Media in the Postpneumococcal Conjugate Vaccine Era. Pediatrics. 2017 Aug 7. [Medline]. 13. Hong W, Peng D, Rivera M, Gu XX. Protection against nontypeable Haemophilus influenzae challenges by mucosal vaccination with a detoxified lipooligosaccharide conjugate in two chinchilla models. Microbes Infect. 2010 Jan. 12 (1):11-8.

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14. Azarpazhooh A, Limeback H, Lawrence HP, Shah PS. Xylitol for preventing acute otitis media in children up to 12 years of age. Cochrane Database Syst Rev. 2011 Nov 9. 11:CD007095. 15. Lieberthal AS, Carroll AE, Chonmaitree T, Ganiats TG, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013 Mar. 131(3):e964- 99. 16. Rosenfeld RM, Schwartz SR, Pynnonen MA, et al. Clinical practice guideline: Tympanostomy tubes in children. Otolaryngol Head Neck Surg. 2013 Jul. 149 (1 Suppl):S1-35. 17. Megged O, Abdulgany S, Bar-Meir M. Does Acute Otitis Media in the First Month of Life Increase the Risk for Recurrent Otitis. Clin Pediatr (Phila). 2018 Jan. 57 (1):89-92. 18. King LM, Bartoces M, Hersh AL, Hicks LA, Fleming-Dutra KE. National Incidence of Pediatric Mastoiditis in the United States, 2000-2012: Creating a Baseline for Public Health Surveillance. Pediatr Infect Dis J. 2018 Mar 27. 1.5 OTITIS MEDIA WITH EFFUSION INTRODUCTION Synonyms: Serous, Secretory, Non suppurative OM, Middle ear effusion, Glue ear OME is defined as the presence of fluid in the middle ear without signs or symptoms of acute ear infection. The non-purulent effusion may either be mucoid or serous. It is commoner in paediatric age group. Chronic OME is defined as presence of middle ear fluid for more than 3 months from the date of onset (if known) or date of diagnosis (if onset unknown). OME may occur during an upper respiratory infection, spontaneously because of poor eustachian tube function or as an inflammatory response following AOM, most often between the ages of 6 months - 4 years Diagnosis Clinical presentations suggestive of possibility of OME in children ü Hearing difficulty (hard of hearing, difficulty to perceive in a group, asking for repetition) ü Recurrent earache ü Delayed speech and language development ü Repeated ear infections ü History of recurrent cold or persistent nasal obstruction

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ü Presence of oro-facial clefts or Down's syndrome ü Behavioral problems, inattention, problem child ü Fall of grades at school ü Infrequently, imbalance and tinnitus Assessment ü Otoscopy should be performed to rule out OME in children with earache, deafness or both. ü Pneumatic otoscopy with visualized & documented presence of middle ear fluid should be the corner stone of diagnosing OME in children. ü If the diagnosis is uncertain after otoscopy, Tympanometry should be obtained in children with suspected OME ü Wax removal must be ensured before tympanometry. Ensure ear canal is free of wax or foreign body. ü Clinicians should obtain an age-appropriate hearing tests if OME persists for ≥3 months OR for OME of any duration in an 'at-risk child' (see below), after ensuring ear canal wax clearance ü Imaging modalities like CT or MRI are not routinely indicated in patients with OME. [However, it may be of value in especially in adults presenting with unilateral OME when a nasopharyngeal lesion or mass compressing eustachian tube must be ruled out.] Note At-risk children- Clinicians should determine if a child with OME is at increased risk for speech, language, or learning problems from middle ear effusion because of baseline sensory, physical, cognitive, or behavioral factors. These include the following: ü Permanent hearing loss (independent of OME) ü Other speech and language disorders ü Autism spectrum disorder / other developmental disorders ü Syndromes (e.g., Down) with cognitive, speech, or language delay ü Blindness or uncorrectable visual impairment ü Cleft palate & other cranio-facial disorders TREATMENT GUIDELINES 1. Clinicians may manage children with OME who is not at-risk with watchful waiting for 3 months from the date of effusion onset (if known) or 3 months from the date of diagnosis (if onset is unknown). This is based on the self-

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limited nature of most OME. 2. Antibiotics, systemic steroids, decongestants or antihistamines are not recommended for treatment of OME. However, may be used in initial conservative management depending on associated clinical situations, up to 3 months in children. 3. Auto inflation using nasal balloons has been beneficial in children with OME in several studies 4. Avoid passive smoking, allergens and feeding infants supine; promote breast feeding 5. For surgical management children with OME may require grommet insertion/ Adenoidectomy Guidelines for grommet insertion for OME a) Grommet insertion may be advised for bilateral OME in children lasting for more than three months despite conservative management, with documented hearing loss [B type tympanogram and / or PTA with more than 40 dB CHL]. b) Clinicians may perform Grommet insertion in children with unilateral or bilateral OME for 3 months AND symptoms attributable to OME that include poor school performance, behavioral problems, ear discomfort, or reduced quality of life. c) Grommet insertion should be offered to all at-risk children right at the time of confirmation of diagnosis of OME. [This is because they are at increased risk for speech, language, or learning problems from middle ear effusion] d) Clinicians should NOT perform grommet insertion in children with a single episode of OME of less than 3 months duration. Guidelines for associated adenoidectomy with grommet insertion a) Clinicians should recommend Grommet insertion, adenoidectomy, or both when surgery is performed for persistent OME in a child 4 years or older. b) Clinicians need recommend grommet insertion alone when surgery is performed for OME in a child < 4 years old; adenoidectomy should be performed in this group only if there is a distinct indication (e.g., severe nasal obstruction, OSAS) other than OME.

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Treatment algorithm for Otitis Media with Effusion (OME)

REFERENCES 1. O'Connor SS, Coggins R, Gagnon L, Rosenfeld RM, Shin JJ, Walsh SA. Plain Language Summary: Otitis Media with Effusion. Otolaryngol Head Neck Surg. 2016 Feb. 154 (2):215-25. 2. Minovi A, Dazert S. Diseases of the middle ear in childhood. GMS Curr Top Otorhinolaryngol Head Neck Surg. 2014. 13: Doc11. 3. Harman NL, Bruce IA, Callery P, Tierney S, Sharif MO, O Brien K, et al. MOMENT -- Management of Otitis Media with Effusion in Cleft Palate: guidelines for a systematic review of the literature and identification of a core outcome set using a Delphi survey. Trials. 2013 Mar 12. 14(1):70. 4. Kubba H, Pearson JP, Birchall JP. The aetiology of otitis media with effusion: a review. Clin Otolaryngol. 2000 Jun. 25(3):181-94. 5. Siddartha, Bhat V, Bhandary SK, Shenoy V, Rashmi. Otitis media with effusion in relation to socio economic status: a community-based study. Indian J Otolaryngol Head Neck Surg. 2012 Mar. 64(1):56-8. 6. Walker RE, Bartley J, Flint D, Thompson JM, Mitchell EA. Determinants of chronic otitis media with effusion in preschool

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children: a case-control study. BMC Pediatr. 2017 Jan 6. 17 (1):4. 7. Pichichero ME, Poole MD. Assessing diagnostic accuracy and tympanocentesis skills in the management of otitis media. Arch Pediatr Adolesc Med. 2001 Oct. 155(10):1137-42. 8. Kaleida PH. Evidence assessment of the accuracy of methods of diagnosing middle ear effusion in children with otitis media with effusion. J Pediatr. 2004 Jul. 145(1):138. 9. Williamson I, Vennik J, Harnden A, et al. Effect of nasal balloon autoinflation in children with otitis media with effusion in primary care: an open randomized controlled trial. CMAJ.2015 Sep 22.187 (13):961-9. 10. Williams RL, Chalmers TC, Stange KC, et al. Use of antibiotics in preventing recurrent acute otitis media and in treating otitis media witheffusion. A meta-analytic attempt to resolve the brouhaha. JAMA. 1993 Sep 15. 270(11):1344-51. 11. Roditi RE, Liu CC, Bellmunt AM, Rosenfeld RM, Shin JJ. Oral Antibiotic Use for Otitis Media with Effusion: Ongoing Opportunities for Quality Improvement. Otolaryngol Head Neck Surg. 2016 May. 154 (5):797-803. 12. Simpson SA, Lewis R, van der Voort J, Butler CC. Oral or topical nasal steroids for hearing loss associated with otitis media with effusion in children. Cochrane Database Syst Rev. 2011 May 11. CD001935. 13. Williamson I, Benge S, Barton S, et al. A double-blind randomized placebo-controlled trial of topical intranasal corticosteroids in 4- to 11- year-old children with persistent bilateral otitis media with effusion in primary care. Health Technol Assess. 2009 Aug. 13(37):1-144. 14. Griffin G, Flynn CA. Antihistamines and/or decongestants for otitis media with effusion (OME) in children. Cochrane Database Syst Rev. 2011 Sep 7. 9:CD003423. 15. Maw R, Bawden R. Spontaneous resolution of severe chronic glue ear in children and the effect of adenoidectomy, tonsillectomy, and insertion of ventilation tubes (grommets). BMJ. 1993 Mar 20. 306(6880):756-60. 16. Boston M, McCook J, Burke B, Derkay C. Incidence of and risk factors for additional tympanostomy tube insertion in children. Arch

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Otolaryngol Head Neck Surg. 2003 Mar. 129(3):293-6. 17. Burton MJ, Rosenfeld RM. Grommets (ventilation tubes) for hearing loss associated with otitis media with effusion in children. Otolaryngol Head Neck Surg. 2006 Oct. 135(4):507-10. 18. Rosenfeld RM, Shin JJ, Schwartz SR, et al. Clinical practice guideline: otitis media with effusion (update). Otolaryngol Head Neck Surg. 2016 Feb. 154 (1 Suppl): S1-S41. 19. Rosenfeld RM, Schwartz SR, Pynnonen MA, et al. Clinical practice guideline: tympanostomy tubes in children. Otolaryngol Head Neck Surg. 2013 Jul. 149 (1 Suppl):S1-35. 20. Simon F, Haggard M, Rosenfeld RM, et al. International consensus (ICON) on management of otitis media with effusion in children. Eur Ann Otorhinolaryngol Head Neck Dis. 2018 Feb. 135 (1S): S33-9. 21. Mills R, Hathorn I. Aetiology and pathology of otitis media with effusion in adult life. J Laryngol Otol. 2016 May. 130 (5):418-24. 22. O'Connor SS, Coggins R, Gagnon L, Rosenfeld RM, Shin JJ, Walsh SA. Plain Language Summary: Otitis Media with Effusion. Otolaryngol Head Neck Surg. 2016 Feb. 154 (2):215-25. 1.6 CHRONIC OTITIS MEDIA INTRODUCTION Chronic Otitis media is long standing inflammation of the middle ear cleft Classification ü Healed COM – Healed perforation (Thin replacement membrane, usually circular in outline; use pneumatic otoscopy to confirm) OR Tympanosclerosis (chalk patches on TM). ü Active Mucosal – Central perforation with middle ear inflammation (mucopus, polyps or granulations in middle ear) ü Active squamosal – Cholesteatoma ü Inactive squamosal – Retraction pockets (either in pars tensa or flaccida) ü Inactive mucosal – Central perforation with normal middle ear Clinical Diagnosis Diagnosis mainstay is history &pneumatic Otoscopy to sub-classify into different types as mentioned above

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Investigations ü Pure tone audiometry – Essential investigation; Look for degree of hearing loss, magnitude of A-B gap, associated sensorineural loss if any and hearing status of the opposite ear ü Culture& sensitivity – Is only of value in active ears especially if suppurative complications are anticipated. Both bacteriological and fungal culture desirable, if unresolved or complicated. ü Radiology – Preferred modality is CT scan; high resolution scan of the temporal bone (axial and coronal sections) is indicated in patients with chronic otitis media and suspected complications, inability to assess the tympanic membrane (e.g. Narrowed canal), disproportionate hearing loss, or in associated congenital anomalies. CT scan may also be considered as an option in patients with chronic otitis media prior to tympano-mastoid surgery. [MRI scan (diffusion weighted non-echo planar images) are recommended in patients with suspected recurrence of cholesteatoma after surgery]. ü Outpatient microscopy / Otoendoscopy – Desirable as it helps to plan surgery and has added advantage as a teaching aid. Aid in preliminary management (aural toilet) as well. MANAGEMENT Healed otitis media 1. Needs no further treatment if hearing is normal. 2. If there is conductive hearing loss of >35 dB the patient may be offered option of Tympanoplasty 3. Informed consent for guarded success in the presence of tympanosclerosis or middle ear adhesions. 4. Hearing aid is an alternative for surgery Mucosal disease 1. Aural toilet and topical antibiotic + topical steroids should be the preliminary management in active ears which aids in better clinical evaluation as well. 2. Topical fluoroquinolones are preferred to aminoglycosides due to theoretical risk of ototoxicity for the latter 3. Appropriate treatment of co morbidities like respiratory allergies, tonsillo- pharyngitis, nasal and sinus disease should be initiated.

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4. Definitive management is tympanoplasty with appropriate ossicular reconstruction. 5. Cortical mastoidectomy need to be added in persistent activity despite adequate initial management. Squamosal disease Inactive Squamosal 1.Adults - If the retraction pocket is stable with no hearing loss regular follow up with microscopic suction clearance as and when necessary should be advised. 2.If there is associated hearing loss of >35db &/ or persistent discharge tympanoplasty need be done. 3.Inactive disease may need surgery in swimmers and hearing aid users. 4.Children - There is a greater likelihood of progression of the pocket. If the hearing is normal frequent follow up need be advised with a low threshold for surgery (in the event of noticing progression of the retraction). If there is hearing loss with a significant pocket a tympanoplasty with appropriate reconstruction should be offered. Active Squamosal 1. Patients with confirmed cholesteatoma need surgery to eradicate the disease, improve the hearing and have a self-cleaning epithelialized ear. 2. Mastoid exploration with appropriate tympanoplasty procedure should be contemplated 3. Type of mastoidectomy may be chosen based on the extent of disease, reliability of the patient, hearing status of the opposite ear, surgeon's experience and surgeon preference. REFERENCES 1. Matsuda Y, Kurita T, Ueda Y, Ito S, Nakashima T. Effect of tympanic membrane perforation on middle-ear sound transmission. J Laryngol Otol. 2009 May. 123 Suppl 31:81-9. 2. Wright D, Safranek S. Treatment of otitis media with perforated tympanic membrane. Am Fam Physician. 2009 Apr 15. 79(8):650, 654. 3. Vikram BK, Khaja N, Udayashankar SG, Venkatesha BK, Manjunath D. Clinico-epidemiological study of complicated and uncomplicated chronic suppurative otitis media. J Laryngol Otol. 2008 May. 122(5):442-6. 4. Meyerhoff WL, Kim CS, Paparella MM. Pathology of chronic otitis media.

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Ann Otol Rhinol Laryngol. 1978 Nov-Dec. 87(6 Pt 1):749-60. 5. Kenna MA. Etiology and Pathogenesis of Chronic Suppurative Otitis Media. Ann Otol Rhinol Laryngol. 1988. 97(Suppl 131):16-17. 6. Matsuda Y, Kurita T, Ueda Y, Ito S, Nakashima T. Effect of tympanic membrane perforation on middle-ear sound transmission. J Laryngol Otol. 2009 May. 123 Suppl 31:81-9. 7. Wright D, Safranek S. Treatment of otitis media with perforated tympanic membrane. Am Fam Physician. 2009 Apr 15. 79(8):650, 654. 8. Van der Veen EL, Schilder AG, van Heerbeek N, et al. Predictors of chronic suppurative otitis media in children. Arch Otolaryngol Head Neck Surg. 2006 Oct. 132(10):1115-8. 9. Vikram BK, Khaja N, Udayashankar SG, Venkatesha BK, Manjunath D. Clinico-epidemiological study of complicated and uncomplicated chronic suppurative otitis media. J Laryngol Otol. 2008 May. 122(5):442-6. 10. Jensen RG, Koch A, Homoe P. The risk of hearing loss in a population with a high prevalence of chronic suppurative otitis media. Int J Pediatr Otorhinolaryngol. 2013 Sep. 77(9):1530-5. 11. Aarhus L, Tambs K, Kvestad E, et al. Childhood Otitis Media: A Cohort Study With 30-Year Follow-Up of Hearing (The HUNT Study). Ear Hear. 2014 Nov 14. 12. Smith JA, Danner CJ. Complications of chronic otitis media and cholesteatoma. Otolaryngol Clin North Am. 2006 Dec. 39(6):1237-55. 13. Sheikh R, Haidar H, Abdulkarim H, et al. Preoperative Predictors in Chronic Suppurative Otitis Media for Ossicular Chain Discontinuity: A Cross- Sectional Study. Audiol Neurootol. 2016. 21 (4):231-6. 14. Dohar JE, Alper CM, Rose EA, Doyle WJ, Casselbrant ML, Kenna MA. Treatment of chronic suppurative otitis media with topical ciprofloxacin. Ann Otol Rhinol Laryngol. 1998 Oct. 107(10 Pt 1):865-71. 15. Consensus Panel, Hannley MT, Dennenny III JC. Use of Ototopical Antibiotics in Treating 3 Common Ear Diseases. Otol Head Neck Surg. 2000. 934-40.

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1.7 PERMANENT CHILDHOOD HEARING LOSS INTRODUCTION Most estimates suggest that 1 to 3 per 1,000 children are born with a hearing loss, based on screening and/or medical records. Aims of management ü To screen all at-risk infants right in the neonatal nursery to rule out hearing loss ü All children to be screened for hearing loss no later than 1 month of age ü Hearing and medical evaluations to be completed no later than 3 months of age ü To fit Infants with confirmed hearing loss with amplification ü Early intervention services to begin no later than 6 months of age ü Early intervention will prevent delays in speech and language development and have long-lasting beneficial effects on social and emotional development and quality of life. ü To engage the parents in various aspects of the evaluation and treatment At-risk neonates to be screened at birth 1. H/O Maternal infections (TORCH) 2. Prematurity 3. Low birth weight 4. Birth injuries/ asphyxia 5. Kern icterus 6. Maternal drug & alcohol abuse 7. Maternal diabetes 8. Toxaemia of pregnancy 9. Anatomical abnormalities of head & neck 10. Genetic syndromes (Treacher Collins, Goldenhar, Alport's, Usher, CHARGE, Waardenburg) Conditions causing permanent hearing loss after birth a. Ear infections b. Ototoxic drugs c. Meningitis/ Encephalitis d. Measles e. Chicken pox

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f. Mumps g. Head injury h. Noise exposure. Screening Neonatal screening a. At risk' neonates require the full test battery even if they pass the initial screen b. To be initiated with otoacoustic emissions at birth in the neonatal nursery. c. Re-test advised in those children who fail the first screen at 3 weeks and 6 weeks. d. If still negative deafness should be confirmed with ABR testing at 3 months of age. e. Infants who pass the neonatal screening but have a risk factor should have a repeat audiology assessment by 24 to 30 months of age. f. Early and more frequent repeat assessments may be indicated for children with maternal TORCH infections, genetic syndromes associated with progressive hearing loss, neuro-degenerative disorders, trauma or postnatal infections like meningitis or with a family history of hearing loss. Note Even if a child passes the new born hearing screening but has risk factors for hearing loss, it is important to consider the need for periodic audiologic monitoring of the child's hearing. This is because of the following reasons i. Mild hearing loss may be missed in screening ii. No screening test is perfect: some children who pass the screening may have hearing loss, and vice-versa iii. Hearing loss can develop after birth (delayed onset or progressive undetected hearing loss) Test battery at 0 - 6 months Otoacoustic emissions, automated ABR, Acoustic immittance measurements (Tympanometry + ASR) Test battery at 6 - 36 months Behavioural observation audiometry (conditioned play audiometry & visual reinforcement audiometry), Speech audiometry, ABR, Otoacoustic

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emissions & Immittance measurements Test battery at 3 – 5 years Pure tone audiometry, speech audiometry, ABR, Otoacoustic emissions & acoustic immittance measurements MANAGEMENT Hearing aids 1. Children with any degree of hearing loss that has the potential to impede access to speech should be made to fit hearing aids as soon as possible; at least within 1 month of diagnosis. 2. Candidates include children with permanent bilateral hearing loss, unilateral hearing loss, auditory neuropathy and cochlear implant candidates as trial amplification period. 3. Behind-the-ear (BTE) is the most commonly recommended type of device for infants and young children. Binaural amplification is to be provided to young children with bilateral hearing loss as far as possible. Cochlear Implant (CI) Children not benefited by hearing aid trial should be counselled for cochlear implantation. Candidacy criteria for CI is as follows: 1. Bilateral severe-to-profound sensorineural hearing loss; 2. Age of 1 year or older (a few exceptions based on aetiology e.g. meningitis) 3. No benefit from binaural hearing aid & intensive auditory training 4. Absence of chronic middle ear pathology, lesions of the VIII cranial nerve& central auditory pathway and other medical issues that contraindicate surgery 5. Family commitment to post-implant rehabilitation process with a realistic expectation for cochlear implant use and benefit. 6. Children diagnosed with Auditory neuropathy / dyssynchrony REFERENCES 1. Barbi M, Binda S, Caroppo S, Ambrosetti U, Corbetta C, Sergi P. A wider role for congenital cytomegalovirus infection in sensorineural hearing loss. Pediatr Infect Dis J 2003 Jan;22(1):39-42 2. Black, F. O., et al. (2001). "A vestibular phenotype for Waardenburg syndrome?" Otol Neurotol 22(2): 188-194. 3. Mafong DD and others. Use of laboratory evaluation and radiologic imaging

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in the diagnostic evaluation of children with sensorineural hearing loss. Laryngoscope 2002:112: 1-7 4. Magliulo G, Iannella G, Gagliardi S, Iozzo N, Plateroti R, Mariottini A, Torricelli F. Usher's Syndrome Type II: A Comparative Study of Genetic Mutations and Vestibular System Evaluation. .Otolaryngol Head Neck Surg. 2017 Nov;157(5):853-860. 5. McClay JE and others. Evaluation of paediatric sensorineural hearing loss with magnetic resonance imaging. Arch ORL 2008:134(9) 945-952 6. Moon, I. S., et al. (2009). "Severe to profound hearing loss in patients with progressed Alport's syndrome." Acta Otolaryngol 129(9): 982-987. 7. Shah, R. K., N. H. Blevins, et al. (2005). "Mid-frequency sensorineural hearing loss: aetiology and prognosis." J Laryngol Otol 119(7): 529-33. 8. Vincent R, Wegener I, Derks LS, Grolman W. Congenital ossicular chain malformations in mobile stapes in children: Results in 17 cases. Laryngoscope. 2016 Mar;126(3):682-8. 9. National Institutes of Health. NIH Consensus Statement. Cochlear Implants in Adults and Children. 1995, May15-17. 13(2):1-30. 10. Gantz BJ, McCabe BF, Tyler RS. Use of multichannel cochlear implants in obstructed and obliterated cochleas. Otolaryngol Head Neck Surg. 1988 Jan. 98(1):72-81. 11. Green JD Jr, Marion MS, Hinojosa R. Labyrinthitis ossificans: histopathologic consideration for cochlear implantation. Otolaryngol Head Neck Surg. 1991 Mar. 104(3):320-6. 12. Biernath KR, Reefhuis J, Whitney CG, et al. Bacterial meningitis among children with cochlear implants beyond 24 months after implantation. Pediatrics. 2006 Feb. 117(2):284-9. [Medline]. 13. Balkany T, Telischi FF. Fixation of the electrode cable during cochlear implantation: the split bridge technique. Laryngoscope. 1995 Feb. 105(2):217-8. [Medline]. 14. Gantz BJ, Tyler RS, Knutson JF, et al. Evaluation of five different cochlear implant designs: audiologic assessment and predictors of performance. Laryngoscope. 1988 Oct. 98(10):1100-6. [Medline]. 15. Das S, Buchman CA. Bilateral cochlear implantation: current concepts. Curr Opin Otolaryngol Head Neck Surg. 2005 Oct. 13(5):290-3.

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1.8 IDIOPATHIC SUDDEN SNHL INTRODUCTION Sudden SNHL is defined as a rapid-onset sensorineural hearing impairment, occurring over a 72-hour period, in one or both ears, with decrease in hearing thresholds of greater than or equal to 30 decibels, affecting at least 3 consecutive frequencies. Idiopathic sudden sensorineural hearing loss (ISSNHL) is defined as SSNHL with no identifiable cause despite adequate investigations Evaluation – Aims & Recommendations ü If audiometry confirms a 30dB hearing loss at 3 consecutive frequencies AND an underlying condition cannot be identified by history and physical examination a presumptive diagnosis of idiopathic Sudden SNHL may be entertained. ü Differentiate conductive from sensorineural hearing loss in all patients presenting with sudden hearing loss. ü Differentiate bilateral sudden hearing loss, recurrent sudden hearing loss and hearing loss as a part of other neurological deficits (from Idiopathic Sudden SNHL) in all patients since the approach should be different. ü Look for clinical features that may be associated with a definable underlying disease at presentation. Among such causes are systemic disorders, autoimmune disorders, metabolic disorders, bilateral Meniere disease, and certain neurological disorders. [see treatment algorithm] ü Retro-cochlear pathology like acoustic neuroma need be ruled out by obtaining an MRI brain or Auditory Brainstem Response (ABR). [CT scan of brain is NOT indicated in the initial evaluation of a patient with presumptive SSNHL]. ü Routine laboratory tests NOT immediately necessary in patients with such presumed ISSNHL to avoid false positives, delay in diagnosis and treatment. MANAGEMENT 1. Systemic corticosteroids should be offered as the initial therapy to patients with ISSNHL. [Suggested treatment regimen would be oral Prednisolone given at 1

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mg/kg/d in a single dose, (maximum dose of 60 mg daily), and treatment duration of 10 to 14 days; full dose may be prescribed for initial 7 days, followed by taper. Alternatively, equivalent doses of Methylprednisolone (48mg daily) may also be used] 2. Antivirals, thrombolytics, vasodilators, vasoactive substances, or antioxidants are NOT 'routinely' indicated in patients with ISSNHL. [However, there may be patient specific indications for each of these options that may be reasonable to try on an individualized basis]. 3. Intra tympanic steroid perfusion may be offered to patients who do not respond to systemic steroids or shows only incomplete response. It is also an option in patients exhibiting intolerance to oral steroids or when systemic steroids are contraindicated. 4. If facilities are available, Hyperbaric oxygen therapy may be suggested to patients with incomplete recovery from ISSNHL after failure of initial management, within three months. Follow up 1. Follow up audiometric evaluation is recommended within 3- 6 months to rule out progressive hearing loss. 2. The clinician should counsel patients with incomplete recovery of hearing about the possible benefits of amplification and other Hearing-assistive technologies for improving communication in specific listening conditions Treatment algorithm for Idiopathic Sudden Sensorineural Hearing Loss (ISSNHL)

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REFERENCES 1. Okamoto M, Shitara T, Nakayama M, et al. Sudden deafness accompanied by asymptomatic mumps. Acta Otolaryngol Suppl. 1994. 514:45-8. 2. Chang SL, Hsieh CC, Tseng KS, et al. Hypercholesterolemia is correlated with an increased risk of idiopathic sudden sensorineural hearing loss: a historical prospective cohort study. Ear Hear. 2014 Mar-Apr. 35(2):256- 61. 3. Rudack C, Langer C, Stoll W, Rust S, Walter M. Vascular risk factors in sudden hearing loss. Thromb Haemost. 2006 Mar. 95(3):454-61. 4. Simmons FB. Theory of membrane breaks in sudden hearing loss. Arch Otolaryngol. 1968 Jul. 88(1):41-8. 5. Toubi E, Ben-David J, Kessel A, Halas K, Sabo E, Luntz M. Immune- mediated disorders associated with idiopathic sudden sensorineural hearing loss. Ann Otol Rhinol Laryngol. 2004 Jun. 113(6):445-9. 6. Sara SA, Teh BM, Friedland P. Bilateral sudden sensorineural hearing loss: review. J Laryngol Otol. 2014 Jan. 128 Suppl 1: S8-15. 7. Passamonti SM, Di Berardino F, Bucciarelli P, et al. Risk factors for idiopathic sudden sensorineural hearing loss and their association with clinical outcome. Thromb Res. 2015 Jan 7. 8. Stachler RJ, Chandrasekhar SS, Archer SM, et al, American Academy of Otolaryngology-Head and Neck Surgery. Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg. 2012 Mar. 146 (3 Suppl):S1-35. 9. Ni Y, Zhao X. [Carbogen combined with drugs in the treatment of sudden deafness]. Lin Chuang Er Bi Yan Hou Ke Za Zhi. 2004 Jul. 18(7):414-5. 10. Wei BP, Mubiru S, O'Leary S. Steroids for idiopathic sudden sensorineural hearing loss. Cochrane Database Syst Rev. 2006 Jan 25. CD003998. 11. Sutton L, Schartinger V, Url C, et al. Intratympanic steroid use for idiopathic sudden sensorineural hearing loss: current otolaryngology practice in Germany and Austria. Eur Arch Otorhinolaryngol. 2018 May. 275 (5):1103-10. 12. Demirhan H, Gokduman AR, Hamit B, Yurekli Altındag MF, Yigit O. Contribution of intratympanic steroids in the primary treatment of sudden hearing loss. Acta Otolaryngol. 2018 Mar 7. 1-4.

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13. Anyah A, Mistry D, Kevern E, Markiewicz K. Idiopathic Sudden Sensorineural Hearing Loss: Average Time Elapsed Before Presentation to the Otolaryngologist and Effectiveness of Oral and/or Intratympanic Steroids in Late Presentations. Cureus. 2017 Dec 14. 9 (12):e1945. 14. Battaglia A, Lualhati A, Lin H, et al. A prospective, multi-centered study of the treatment of idiopathic sudden sensorineural hearing loss with combination therapy versus high-dose prednisone alone: a 139-patient follow-up. Otol Neurotol. 2014 Jul. 35(6):1091-8. 15. Tsounis M, Psillas G, Tsalighopoulos M, Vital V, Maroudias N, Markou K. Systemic, intratympanic and combined administration of steroids for sudden hearing loss. A prospective randomized multicenter trial. Eur Arch Otorhinolaryngol. 2018 Jan. 275 (1):103-10. 16. Lee JW, Park YA, Park SM, et al. Clinical Features and Prognosis of Sudden Sensorineural Hearing Loss Secondary to Intralabyrinthine Hemorrhage. J Audiol Otol. 2016 Apr. 20 (1):31-5. 17. Kang WS, Yang CJ, Shim M, et al. Prognostic Factors for Recovery from Sudden Sensorineural Hearing Loss: A Retrospective Study. J Audiol Otol. 2017 Apr. 21 (1):9-15. 18. Fetterman BL, Saunders JE, Luxford WM. Prognosis and treatment of sudden sensorineural hearing loss. Am J Otol. 1996 Jul. 17(4):529-36. 19. Wilson WR. The relationship of the herpesvirus family to sudden hearing loss: a prospective clinical study and literature review. Laryngoscope. 1986 Aug. 96 (8):870 - 77. 1.9 BELL'S PALSY INTRODUCTION Bell's palsy is defined as rapid onset (within 72 hours) of unilateral LMN facial palsy. (Bilateral Bell's palsy is rare). It is the most common cause of acute LMN Facial palsy Diagnostic guidelines ü Bell's palsy is diagnosed when no other aetiology is identified as a cause of the facial weakness. ü It is a diagnosis of exclusion requiring the careful elimination of other causes of facial paresis or paralysis. ü Other conditions causing facial paralysis, include stroke, brain tumours, parotid tumours, facial nerve malignancies, ear infections and systemic

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diseases including Herpes zoster, sarcoidosis, and Lyme disease (see treatment algorithm) ü Bell's palsy has been observed to be commoner in 15-45 age group, those with diabetes, immunocompromise or during pregnancy. ü Preceding upper respiratory catarrh has been reported. ü Bell's palsy is typically self-limiting Management guidelines 1. Detailed evaluation with history and physical examination to exclude identifiable causes of facial paralysis is recommended in all patients presenting with acute onset unilateral facial paralysis. 2. Laboratory testing or diagnostic imaging is not routinely indicated in patients thus diagnosed with Bell's palsy. 3. Oral steroids are indicated within 72 hours of onset of symptoms in patients with Bell's palsy. 4. Oral antiviral therapy may be offered in addition to oral steroids within 72 hours of onset of facial paralysis in patients with Bell's palsy. 5. Eye care precautions should be carried out in patients with Bell's palsy presenting with impaired eye closure. 6. Electrodiagnostic testing is not recommended for patients with Bell's palsy with incomplete facial paralysis; however, electrodiagnostic testing may be offered to patients with complete facial paralysis since it can provide meaningful prognostic information. 7. Surgical decompression is not routinely indicated. However, the need for the same must be individualized based on the level of recovery of facial nerve function after onset of palsy. Definite recommendation is not possible due to lack of strong evidence. 8. Physiotherapy is not routinely recommended in patients with Bell's palsy due to lack of evidence favoring its benefit or harm. 9. Imaging and neurology reference are recommended in patients with new or worsening neurologic findings, progression of paralysis or incomplete facial recovery even after three months following onset of symptoms.

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Treatment algorithm for Bell's Palsy

REFERENCES 1. Baugh RF, Basura GJ, Ishii LE, Schwartz SR, Drumheller CM, Burkholder R, et al. Clinical Practice Guideline: Bell's Palsy Executive Summary. Otolaryngol Head Neck Surg. 2013 Nov. 149(5):656-63. 2. Gronseth GS, Paduga R. Evidence-based guideline update: steroids and antivirals for Bell palsy: report of the Guideline Development 3. Subcommittee of the American Academy of Neurology. Neurology. 2012 Nov 27. 79(22):2209-13. 4. Vrabec JT, Backous DD, Djalilian HR, Gidley PW, Leonetti JP, Marzo SJ, et al. Facial Nerve Grading System 2.0. Otolaryngol Head Neck Surg. 2009 Apr. 140(4):445-50. 5. Katusic SK, Beard CM, Wiederholt WC, Bergstralh EJ, Kurland LT. Incidence, clinical features, and prognosis in Bell's palsy, Rochester, Minnesota, 1968- 1982. Ann Neurol. 1986 Nov. 20(5):622-7. 6. Gronseth GS, Paduga R. Evidence-based guideline update: Steroids and antivirals for Bell palsy: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2012 Nov 7. 7. Sullivan FM, Swan IR, Donnan PT, Morrison JM, Smith BH, McKinstry B, et al. Early treatment with prednisolone or acyclovir in Bell's palsy. N Engl J Med.

47 Section I STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES

2007 Oct 18. 357(16):1598-607. 8. Engström M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valaciclovir in Bell's palsy: a randomised, double-blind, placebo- controlled, multicentre trial. Lancet Neurol. 2008 Nov. 7(11):993-1000. 9. Seok JI, Lee DK, Kim KJ. The usefulness of clinical findings in localising lesions in Bell's palsy: comparison with MRI. J Neurol Neurosurg Psychiatry. 2008 Apr. 79(4):418-20. 10. Murakami S, Mizobuchi M, Nakashiro Y, Doi T, Hato N, Yanagihara N. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med. 1996 Jan 1. 124(1 Pt 1):27- 30. 11. Unlu Z, Aslan A, Ozbakkaloglu B, Tunger O, Surucuoglu S. Serologic examinations of hepatitis, cytomegalovirus, and rubella in patients with Bell's palsy. Am J Phys Med Rehabil. 2003 Jan. 82(1):28-32. 12. Kawaguchi K, Inamura H, Abe Y, Koshu H, Takashita E, Muraki Y, et al. Reactivation of herpes simplex virus type 1 and varicella-zoster virus and therapeutic effects of combination therapy with prednisolone and valacyclovir in patients with Bell's palsy. Laryngoscope. 2007 Jan. 117(1):147-56. 13. Lee AG, Brazis PW, Eggenberger E. Recurrent idiopathic familial facial nerve palsy and ophthalmoplegia. Strabismus. 2001 Sep. 9(3):137-41. 14. Grogan PM, Gronseth GS. Practice parameter: Steroids, acyclovir, and surgery for Bell's palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001 Apr 10. 56(7):830-6. 15. Teixeira LJ, Valbuza JS, Prado GF. Physical therapy for Bell's palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2011 Dec 7. CD006283. 16. Cardoso JR, Teixeira EC, Moreira MD, Fávero FM, Fontes SV, Bulle de Oliveira AS. Effects of exercises on Bell's palsy: systematic review of randomized controlled trials. Otol Neurotol. 2008 Jun. 29(4):557-60.

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1.10.MÉNIÈRE'S DISEASE INTRODUCTION Definition Ménière's disease is defined as recurrent, spontaneous episodic vertigo, hearing loss, aural fullness and tinnitus caused by endolymphatic hydrops Diagnostic Criteria for diagnosis of Meniere's Disease 1. Two or more spontaneous episodes of vertigo, each lasting 20 mins to 12 hours 2. Audiometrically documented low- to mid-frequency sensorineural hearing loss in one ear, on at least one occasion before, during, or after the episode of vertigo 3. Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the affected ear 4. Not better accounted for by another vestibular diagnosis ü Investigations ü Pure tone audiogram – Predominantly low frequency SNHL during early stages; involvement of other frequencies occurs as disease progress. Evidence of recruitment may be elicited. ü The following may also be done if diagnosis is in doubt Ø Electrocochleography (if available) – Shows SP/AP ratio > 35 Ø Investigations to rule out other causes of endolymphatic hydrops - Include serum TSH, ESR, VDRL, Lipid profile Ø MRI brain - to rule out retro-cochlear pathology like CP angle lesions & multiple sclerosis MANAGEMENT Advices Low salt diet, avoidance of alcohol, smoking, caffeine, chocolates, cola, junk food and water restriction during acute attack Therapy during acute episode 1. Rest 2. Anxiolytics (Diazepam) 3. Labyrinthine sedatives (Promethazine, Meclizine, Cinnarizine 4. Anti-emetics (Scopolamine)

49 Section I STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES

Drug treatment in established cases 1. Drugs to lower endolymph pressure - Hydrochlorothiazide, Acetazolamide 2. Anti-inflammatory (if autoimmune aetiology suspected) – Corticosteroids (May also be delivered as intra-tympanic injections if systemic steroids cannot be tolerated or are contraindicated) 3. Intra-tympanic Gentamycin – Effective in majority of cases; ideal in unilateral disease in older individuals. (Warn patients about potential danger of cocohleotoxicity) 4. Surgical options, in patients unresponsive to drug treatment or Intra- tympanic therapy a. Vestibular neurectomy, Endolymphatic shunt surgery b. Labyrinthectomy -In unilateral disease REFERENCES 1. Ronstein A, Lempert T. Dizziness. A practical approach to diagnosis and management. Cambridge University Press, 2007. 2. Fiorino F, Pizzini FB. MRI performed after intratympanic gadolinium administration in patients with Meniere's disease. Correlation with symptoms and signs. Eur Arch Otolaryngol2011; 268:181-7. 3. Harris JP, Alexander TH. Current-day prevalence of Meniere's syndrome. Audiol Neurootol2010; 15:318-22. 4. Thomas K, Harrison MS. Long-term follow-up of 610 cases of Meniere's Disease. Proc R Soc Med1971; 64:853-7. 5. Kentala E. Characteristics of six otological diseases involving vertigo. Am J Otol1996; 17:883-892. 6. Silverstein H, Smouha E, Jones R. Natural history vs surgery for Ménière's disease. Otolaryngol Head Neck Surg1989; 100:6-16. 7. Odkvist LM, Bergenius J. Drop attacks in Meniere's disease. Acta Otolaryngol1988; 455:82-5. 8. Naftalin L, Harrison MS. Vertigo. J Laryngol Otol 1963; 77:827-34. 9. James A, Burton MJ. Betahistine for Ménière's disease or syndrome. Cochrane Database Syst Rev2001;1:CD001873. 10. Burgess A, Kundu S.Diuretics for Ménière's disease or syndrome. Cochrane Database Syst Rev2006;3:CD003599. 11. Garduño-Anaya MA, Couthino De Toledo H, Hinojosa-González R, Pane- Pianese C, Ríos-Castañeda LC. Dexamethasone inner ear perfusion by

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intratympanic injection in unilateral Meniere's disease: a two-year prospective, placebo-controlled, double-blind, randomized trial. Otolaryngol Head Neck Surg2005; 133:285-94. 12. Boleas-Aguirre MS, Lin FR, Della Santina CC, Minor LB, Carey JP. Longitudinal studies with intra-tympanic dexamethasone in the treatment of Meniere's Disease. Otol Neurotol 2008; 29:33-8.14 13. Chia SH, Gamst AC, Anderson JP, Harris JP. Intratympanic gentamicin therapy for Meniere's disease: a meta-analysis. Otol Neurotol 2004; 25:544- 52. 14. Thomsen J, Bretlau P. Placebo effect in surgery for Meniere's disease. A double-blind, placebo-controlled study on endolymphatic sac shunt surgery. Arch 1.11. BENIGN PAROXYSMAL POSITIONAL VERTIGO INTRODUCTION Benign paroxysmal positional vertigo (BPPV) is probably the most common cause of vertigo; it has been estimated that at least 20% of patients who present with vertigo have BPPV. BPPV is characterized by recurrent episodes of rotational vertigo, often severe in intensity, precipitated by change in position of the head and neck in relation to the gravity vector, associated with severe nausea and vomiting, in the absence of auditory symptoms Diagnosis ü Rule out other causes of vertigo (see treatment algorithm) by clinical evaluation. ü The Dix-Hallpike positional test is the standard clinical test for BPPV. The finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic of posterior canal BPPV. The nystagmus induced by Dix-Hallpike test is typically torsional and up- beating; clockwise in left ear and anticlockwise in the right. ü Lateral canal BPPV is suspected if the patient has a history compatible with BPPV and the Dix-Hallpike test exhibits horizontal or no nystagmus. ü Supine head-roll test is used to diagnose the rarer lateral canal variant of BPPV. When the patient is rolled to the affected side, there is intense horizontal nystagmus beating to the under most (affected) ear [geotropic nystagmus]. When the patient is rolled to the healthy (nonaffected) side,

51 Section I STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES

there is a less intense horizontal nystagmus again beating toward the under most ear. ü Positional tests also help to differentiate BPPV from central lesions like cerebellar infarction & brainstem tumours. ü Vestibular testing is not routinely indicated in a patient who meets diagnostic criteria for BPPV in the absence of additional vestibular signs and/or symptoms inconsistent with BPPV. ü Laboratory studies are not recommended in routine diagnosis. ü MR imaging may be used to rule out positional vertigo of central origin; however, patients who meets diagnostic criteria for BPPV in the absence of additional signs and/or symptoms inconsistent with BPPV do not warrant imaging. Note Indications for Radiographic imaging of the CNS ü Patients with suspected BPPV but inconclusive positional testing ü Patients with clinical history compatible with BPPV but also demonstrate added neurologic symptoms atypical for BPPV like headache and visual disturbances. ü Patients with other neurologic signs on physical examination that are not typically associated with BPPV like cranial nerve palsies or meningeal irritation. TREATMENT GUIDELINES 1. BPPV should be treated by canalolith repositioning manoeuvre (CRP); since the benefit-to-risk ratio is very high, it is the obvious first choice among treatment modalities. 2. Post-procedural postural restrictions are NOT needed after CRP for posterior canal BPPV; (these include sleeping upright, lying on the involved side, or use of a cervical collar). 3. Clinicians should not routinely treat BPPV with vestibular suppressant medications. However, these drugs may be used in short-term management of autonomic symptoms such as nausea / vomiting, in patients who are severely symptomatic yet refuse therapy or in patients who become severely symptomatic after CRP. 4. Vestibular rehabilitation exercises, (either self-administered or by the

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clinician), may be offered as an option in the treatment of BPPV. It may be considered, in patients with persistent disability following CRP, refuse CRP, or are not candidates for CRP. Surgery has very limited role in management of BPPV Treatment algorithm for BPPV

REFERENCES 1. Anagnostou E, Kouzi I, Spengos K. Diagnosis and Treatment of Anterior- Canal Benign Paroxysmal Positional Vertigo: A Systematic Review. J Clin Neurol. 2015 May 28. 2. Epley JM. New dimensions of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 1980 Sep-Oct. 88(5):599-605 3. Tirelli G, Nicastro L, Gatto A, Tofanelli M. Repeated canalith repositioning procedure in BPPV: Effects on recurrence and dizziness prevention. Am J Otolaryngol. 2017 Jan - Feb. 38 (1):38-43. 4. Shim DB, Kim JH, Park KC, Song MH, Park HJ. Correlation between the head-lying side during sleep and the affected side by benign paroxysmal positional vertigo involving the posterior or horizontal semicircular canal. Laryngoscope. 2012 Feb 16. 5. Bhattacharyya N, Gubbels SP, Schwartz SR, et al. Clinical Practice Guideline: Benign Paroxysmal Positional Vertigo (Update). Otolaryngol Head Neck Surg. 2017 Mar. 156 (3_suppl): S1-S47.

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6. Picciotti PM, Lucidi D, De Corso E, Meucci D, Sergi B, Paludetti G. Comorbidities and recurrence of benign paroxysmal positional vertigo: personal experience. Int J Audiol. 2016 May. 55 (5):279-84. 7. Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2008 May 27. 70(22):2067-74. 8. Fung K, Hall SF. Particle repositioning maneuver: effective treatment for benign paroxysmal positional vertigo. J Otolaryngol. 1996 Aug. 25(4):243-8. 9. Weider DJ, Ryder CJ, Stram JR. Benign paroxysmal positional vertigo: analysis of 44 cases treated by the canalith repositioning procedure of Epley. Am J Otol. 1994 May. 15(3):321-6. 10. Messina A, Casani AP, Manfrin M, Guidetti G. Italian survey on benign paroxysmal positional vertigo. Acta Otorhinolaryngol Ital. 2017 Aug. 3

54 Section II Common diseases of Nose

STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section II

Section II 2.1. RHINOSINUSITIS SCOPE: This guideline is designed to focus all specialists involved in management of acute/chronic rhinosinusitis (bacterial/fungal) in the secondary or tertiary care level to ensure standard scientific management. This includes the guidelines for accurate diagnosis, prompt identification of complications and scientific management. The guideline is intended for all clinicians who are likely to diagnose and manage adults with rhinosinusitis and applies to secondary or tertiary care setting in which an adult with rhinosinusitis would be identified, monitored, or managed. This guideline, however, does not apply to patients of any age with complicated rhinosinusitis and does not include guidelines for surgical management KEY WORDS: Adult sinusitis, rhinosinusitis 2.1.1 INTRODUCTION: Rhinosinusitis in adults is defined as inflammation of the nose and the paranasal sinuses Rhinosinusitis may be classified by duration as ü Acute rhinosinusitis (ARS) if less than 4 weeks' duration ü Chronic rhinosinusitis (CRS) if lasting more than 12 weeks, with or without acute exacerbations. ü Rhinosinusitis lasting 4-12weeks, being rare decisions about whether such patients are more like ARS or CRS must be individualized. ARS may be classified further by presumed aetiology, based on symptoms and time course as ü Acute bacterial rhinosinusitis (ABRS) or ü Viral rhinosinusitis (VRS) 2.1.2.ACUTE RHINOSINUSITIS Diagnostic recommendations ü Purulent (not clear) nasal or post-nasal discharge with nasal obstruction, facial pain-fullness, or both ü Nasal obstruction or facial pain without purulent nasal drainage is not consistent with ARS ü Acute bacterial rhinosinusitis is diagnosed when

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Ø Symptoms or signs fail to improve within 10 days or more beyond the onset or worsen after initial improvement (double sickening) within 10 days Ø Fever, cough, fatigue, hyposmia or anosmia, maxillary dental pain or ear fullness may be present Ø Elevated ESR, CRP Ø Anterior rhinoscopy may reveal nasal inflammation, purulent discharge, mucosal oedema and structural abnormalities if present Investigations ü Imaging, haematological and microbiological investigations and endoscopy are not routinely required in the diagnosis of ARS, but may be done in high-risk patients ü Elevated ESR and CRP in Acute bacterial rhinosinusitis ü Imaging may be done ü When a complication of ABRS (orbital, intra-cranial or soft tissue involvement) or ü An alternative diagnosis (non-infectious cause of facial pain or malignancy) is suspected or ü When the patient has modifying factors or co-morbidities that predispose to complications, including diabetes, immune-compromised state, history of facial trauma or surgery TREATMENT GUIDELINES Acute rhinosinusitis 1. Analgesics, intranasal corticosteroids, saline irrigation (for symptom relief) 2. Topical decongestant should not be used continuously for more than 3-5 days because of their propensity to cause rebound congestion and rhinitis medicamentosa 3. No indication for the use of antihistamines (both intranasal & oral) except in co-existing allergy 4. Watchful waiting policy may be tried for seven days before starting antibiotic therapy in mild-moderate ABRS only if follow-up is assured 5. Antibiotic therapy in ABRS a) High dose Amoxycillin (90mg/kg/day in 2 divided doses) is the antibiotic of choice for 5-10 days with follow-up

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b) Amoxycillin – clavulanate may be given as first line to those at a high risk of being infected by an organism resistant to Amoxycillin, in moderate-severe infection, with other co-morbidities c) In case of penicillin allergy, Doxycycline, Levofloxacin or Azithromycin for 5-10 days 6. If patient fails to improve with antibiotic therapy by seven days after diagnosis or worsen during initial management, endoscopy directed culture from middle meatus and start empirically on second line drugs (Levofloxacin 500mg daily) 7. Reassess to exclude other causes or complications 2.1.3 CHRONIC RHINOSINUSITIS (with or without nasal polyps) in adults: Chronic rhinosinusitis (CRS) is a complex disease, with a pathophysiology that is likely to be affected by multiple factors including genetic and environmental. Diagnostic recommendations ü Presence of two or more symptoms one of which should be nasal obstruction or nasal discharge (anterior or post-nasal drip) with or without ü Facial pain/pressure ü Hyposmia/anosmia ü For >12wks ü With demonstrable disease - Either endoscopic signs of nasal polyps, and / or oedema / mucopurulent discharge primarily from middle meatus and / or CT changes; mucosal changes in the OMC or sinuses ü Normal nasal endoscopy makes it very unlikely that a patient's facial pain is due to rhinosinusitis Investigations: ü Nasal endoscopic evaluation ü CT scan nose & PNS in severe disease, to exclude malignancy, or before planning for surgery ü In the absence of symptoms, diagnosis of CRS based on radiology alone is inappropriate. ü Tissue biopsy is required to confirm diagnosis in polyp and to exclude from other pathologies especially in unilateral polyp ü Assess the patient with chronic rhinosinusitis for multiple chronic conditions that would modify management such as asthma, cystic fibrosis, immunocompromised state and ciliary dyskinesia.

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TREATMENT GUIDELINES Chronic Rhinosinusitis CRS without polyp: 1. Mild- intranasal corticosteroid with saline nasal irrigation 2. If improvement, continue intranasal corticosteroid, reduce the dose to minimum possible and follow-up 3. If there is no improvement after three months / moderate-severe with mucosal disease on endoscopy – intranasal corticosteroids with nasal saline irrigation and consider long-term antibiotics (Azithromycin/ Clarithromycin for 6-12weeks) 4. When considering long-term macrolide treatment, a serum IgE is helpful in trying to identify likely responders (Patients with normal IgE respond to long term antibiotic therapy) 5. Do CT scan PNS if not done before and consider surgery 6. After surgery, follow up with saline irrigations and intranasal corticosteroids Chronic rhinosinusitis with polyp A. Mild 1. Intranasal corticosteroid spray with nasal saline irrigation 2. Review after three months 3. If there is improvement, continue the same treatment and review every six months B. Moderate with mucosal disease at endoscopy 1. Intranasal corticosteroid spray with saline irrigation - Consider increasing the dose of spray 2. Consider long term antibiotic (Doxycycline 100mg per day for 3 weeks) 3. If improvement, follow-up with intranasal corticosteroid 4. If no improvement, do radiological evaluation and proceed with surgery. C. Severe with mucosal disease at endoscopy 1. Apart from intranasal corticosteroid with saline spray, start a short course of oral corticosteroid. 2. If no improvement after one month, do radiological evaluation, surgery & follow up. 3. Consider urgent investigation and intervention if there is evidence of complications.

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2.1.4 CHRONIC RHINOSINUSITIS IN CHILDREN The four most common symptoms are cough, rhinorrhoea, nasal congestion and post nasal drip with a slightly higher predominance of chronic cough. The adenoids are a predominant contributor to CRS in young children. Management is similar. 1. Nasal corticosteroid treatment is a first line treatment in CRS with and without nasal polyps in children 2. In moderate-severe cases or in mild cases without improvement after maximal medical therapy, consider adenoidectomy alone/with maxillary sinus wash or balloon dilatation 3. Radiological evaluation &FESS is indicated in further persistence of symptoms (Lund-Mackay score >5) 4. FESS is the initial surgical option in with cystic fibrosis, nasal polyposis, antro-choanal polyposis, or AFS 2.1.5 ALLERGY AND RHINOSINUSITIS: If allergy testing is positive and appears clinically relevant based on individual assessment management 1. Environmental control measures, pharmacotherapy or immunotherapy as an immunomodulating approach. 2. The clinician may obtain testing for allergy or immune function in evaluating a patient with CRS or acute / recurrent rhinosinusitis when aggressive management has failed or when sinusitis is associated with otitis media, bronchiectasis or pneumonia 2.1.6 FUNGAL RHINOSINUSITIS: Incidence of fungal rhinosinusitis is on the rise. Ø Diagnosis - classified into invasive and non-invasive based on presence or absence of tissue invasion by fungal hyphae Ø Invasive: Acute invasive, chronic invasive, chronic granulomatous invasive Ø Non-invasive: Saprophytic fungal infestation, fungal ball, and fungus related eosinophilic rhinosinusitis including AFRS Clinical signs of suspicion: ü Unresolved rhinosinusitis even after adequate antibiotic therapy ü Extensive intranasal sloughing ü Numbness of cheek

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ü Diminution or loss of vision on side of involvement ü External ophthalmoplegia on side of involvement ü Black eschar in nasal mucosa ü Palatal blanching especially unilateral ü Uncontrolled Diabetes mellitus with ketoacidosis, signs of renal impairment, immunocompromised patient Invasive fungal sinusitis: Diagnostic criteria: ü Histopathological demonstration of fungal hyphae in mucosa, sub- mucosa, bone or blood vessel, positive fungal smear on fungal staining (GMS staining is the most sensitive in identifying fungi) plus or minus radiologic evidence of sinusitis. ü CT scan may be negative in early cases. MRI is complementary ü Fungal culture remains the gold standard, which may not be rewarding always Acute invasive: Acute invasive fungal rhinosinusitis is the terminology preferred to fulminant, or necrotizing fungal rhinosinusitis ü Disease of < 4 weeks duration in immunocompromised patients ü High index of suspicion is needed for early diagnosis ü This is the most dangerous and life-threatening form of fungal sinusitis ü Usually caused by saprophytic fungi of the order Mucorales, including Rhizopus, Rhizomucor, Absidia, Mucor, Cunninghamella, Morteirella and Apophysomyces species and also by Aspergillus. ü Seen in immunocompromised patients and very rarely in immunocompetent individuals. Apophysomyces elegans causes acute invasive rhinosinusitis in immunocompetent individuals. ü Early physical findings on endoscopy include pallor of mucosa; decreased bleeding on abrasion of mucosa. ü Later black eschar with necrosis develops which can extent to palate. Treatment: Must be started as soon as provisional diagnosis is made which includes 1. Surgical debridement to remove all necrotic tissues which may be repeated 2. Appropriate anti-fungal therapy (Amphotericin / Voriconazole)

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3. Reversal of immunocompromised state wherever possible 4. Long term follow-up Chronic invasive: ü Seen in subtle immunocompromised state like elderly diabetic. ü Patients present with symptoms of long-standing sinusitis over at least 3 months duration. ü Symptoms are usually not acute; fever and mental status changes are absent. ü Commonly caused by Aspergillus fumigatus, occasionally mucor. Treatment: Surgical debridement, antifungal therapy and long-term follow-up Chronic Granulomatous Invasive Rhinosinusitis: ü Relatively rare. ü Usually seen in immunocompetent individuals. ü Usually caused by Aspergillus flavus. ü Disease has a relatively slow time course over three months ü Patients present with an enlarging mass in the cheek, orbit, nose and sinuses. Treatment: Surgical debridement, anti-fungal therapy and long-term follow-up. ANTIFUNGAL THERAPY Invasive aspergillosis / invasive candidiasis Primary therapy Voriconazole (6mg/kg IV every 12 hr for one day, followed by 4mg/kg IV every 12hr; oral dosage is 200mg every 12hr) Alternate therapy 1. Conventional Amphotericin B(if tolerated)(0.5-1.5mg/Kg/day),L-AMB (3- 5mg/kg/day IV), ABLC (5mg/kg/day IV), Posaconazole (200mg qid initially and then 400mg bid orally after stabilization of diseased), Itraconazole(100-200mg bd) 2. Caspofungin (70mg day1 IV and 50mg/day thereafter) in salvage cases Invasive Mucor Rhinosinusitis Liposomal amphotericin or conventional amphotericin (if tolerated) remains to be the drug of choice with or without itraconazole, voriconazole

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Non- invasive Fungal Rhinosinusitis Fungal ball ü Extra mucosal masses of fungal hyphae without any evidence of invasion. ü Commonly caused by Aspergillus. ü Usually single sinus is involved. ü Most commonly involved sinuses are maxillary and sphenoid sinuses Treatment: 1. Removal of fungal ball through endoscopic sinus surgery. 2. Antifungal treatment is not recommended. Allergic Fungal Rhinosinusitis ü Allergic reaction to aerosolized environmental fungi ü Usually of the Dematiaceous species ü In immunocompetent host. Diagnostic criteria Patients with allergic fungal rhinosinusitis (AFRS) normally presents with ü Signs and symptoms of nasal airway obstruction, allergic rhinitis or chronic sinusitis. ü Type 1 (IgE mediated) hypersensitivity to fungi ü Nasal polyposis ü Characteristic hetero-dense radiographic findings ü Eosinophilic mucin without fungal invasion into sinus tissue ü Positive fungal stain of sinus contents removed at the time of surgery. Treatment: 1. Endoscopic sinus surgery to clear polypi and allergic mucin and to restore the ventilation and drainage of sinuses. 2. This must be combined with aggressive medical therapy with corticosteroids which can be given nasally and / or systemically. 3. Patient may also benefit from immunotherapy and antihistamines. 4. Antifungal therapy is usually not required as it is the reaction to the fungus that needs to be treated. 5. However, in severe recalcitrant disease, antifungal therapy may be needed.

64 Flowchart for management of sinusitis is given below

RHINOSINUSITIS Chronic ((> 12> 12 weeks) weeks) [CRS] [CRS] Acute ( < 4 weeks) [ARS]

ST

ANDARD TREA Viral Bacterial

 Analgesics

 Intranasalsteroids Start antibiotic TMENT GUIDELINES  Antihistamines in case of allergy

 Co-amoxiclav No improvement  Macrolides Super-added (5-10 days) bacterial infection ON COMMONEARDISEASES No improvement / Improvement W orsening / Complications

CT PNS Nasal endoscopy C & S Change antibiotic Toconfirmdiagnosis & exclude complications

Section II 65 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section II

66 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section II

67 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section II

REFERENCES 1. Fokkens W, Lund V, Mullol J. EP3OS 2007: European position paper on rhinosinusitis and nasal polyps 2007. A summary for otorhinolaryngologists. Rhinology. 2007 Jun;45(2):97-101. 2. Meltzer EO, Hamilos DL. Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines. Mayo Clinic proceedings Mayo Clinic. 2011 May;86(5):427-43 3. Wang DY, Wardani RS, Singh K, Thanaviratananich S, Vicente G, Xu G, et al. A survey on the management of acute rhinosinusitis among Asian physicians. Rhinology. 2011 Sep;49(3):264-71. Arunaloke Chakrabarti 4. , MD et.al. Fungal Rhinosinusitis: A Categorization and Definitional Schema Addressing Current Controversies: Laryngoscope.2009 Sept;119(9):1809-1818 5. Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the Infectious Diseases Society of America: Clin Infect Dis.2016 Aug 15; 63(4): e1–e60 6. Harvey R, Hannan SA, Badia L, Scadding G. Nasal saline irrigations for the symptoms of chronic rhinosinusitis. Cochrane database of systematic reviews (Online).2007(3):CD006394. 7. Clinical Practice guidelines- American academy of otorhinolaryngology Head-Neck surgery 2015 2.2. EPISTAXIS SCOPE This guidelines is applicable to all medical staff involved in the management of epistaxis. This guideline will act as a reference in secondary and tertiary care hospitals and primary care centers, available to all clinicians involved in the patient management. This guideline includes general management strategy and detailed diagnostic and therapeutic guidelines for conditions causing epistaxis. Aim To develop criteria for management of patients attending emergency medicine department with epistaxis

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Definition The management of patient with epistaxis comprises two concurrent processes- diagnostic and therapeutic culminating in decision to either conservatively manage or to interfere operatively. INTRODUCTION Epistaxis is just a symptom and majority causes are idiopathic. It can be torrential requiring emergency management or can be mild. The causes of epistaxis are many, but common causes are 1. Inflammatory diseases- viral upper respiratory infection, bacterial sinusitis, allergic rhinitis, environmental irritants 2. Traumatic 3. Neoplasm- malignancy-suspected especially in elderly 4. Benign-Vascular malformation, haemangioma, juvenile nasopharyngeal angiofibroma 5. Structural- Nasal septal deformity with spurs, septal perforation 6. Systemic–Coagulation deficits like thrombocytopenia, Coagulopathies, Liver disease, renal failure, chronic alcohol abuse etc. 7. Vascular diseases- arteriosclerotic, Hereditary haemorrhagic telangiectasia 8. Cardiovascular conditions - Hypertension The most common site of hemorrhage is Little's area in the septum in young adults. In elderly the causes are usually arteriosclerosis in association with hypertension and malignancy. Treatment guidelines Initial evaluation involves Assessment of haemo-dynamic stability and potential airway compromise of the patient including a quick visual assessment, review of vital signs and laboratory studies that may have been obtained Management aims at ü Resuscitation ü Establish the site and diagnosis ü Management of bleeding & the cause

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Primary care centres Then aim of primary care physician should be to stop the bleeding and refer the patient to higher centers for further management. If the bleeding stops by itself, they can manage the cause as established. The bleeding can be stopped by ü Pinching the nose (Trotter's position) ü Cold compresses ü Controlling blood pressure if high ü Propped up position ü Stop antiplatelet drugs, anticoagulants, NSAIDs (if patient is on these) ü IV access. Patient should be reassured & explained about the planned evaluation and possible treatment ü Topical nasal decongestants. If bleeding does not stop, hemostatic injection like Inj. Tranexamic acid 1amp in 100 ml NS slow IV or Inj. Ethamsylate 1amp iv can be tried. ü If bleeding persists, nasal packs are needed. Anterior nasal packing can be given, and the patient referred to higher centers Referral criteria ü If bleeding is severe enough which is not controlled by external digital pressure ü Uncontrolled blood pressure ü Associated faciomaxillary injury ü If bleeding is associated with nasal mass (rhinosporidiosis / malignancy) ü If it is unprovoked bleeding especially in adolescent males (JNA to be ruled out) ü If associated with unilateral foul-smelling nasal discharge in a child (suspected foreign body) ü Recurrent nasal bleeding in an elderly ü Coagulopathies ü Post-surgery bleed

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Secondary care: History and examination The experienced ENT surgeon or senior or junior resident see the case in ENT casualty and provide early assessment and investigations to reduce unnecessary admissions. Based on detailed history and examination, ENT consultant can arrive at various possibilities and order necessary investigations. Investigations Hb, CBC, RBS BT, CT, PT-INR, APTT RFT, LFT, Peripheral smear, Blood grouping and cross matching Depending on nasal examination - CT scan Nose & PNS + diagnostic nasal endoscopy Treatment Depends on clinical diagnosis. ü May be viewed as a continuum ranging from no intervention with only conservative treatment to invasive surgical and angiography procedures ü Admit those with not much control of bleeding. In most patients bleeding responds to nasal packing or cauterization. Medical approaches are 1. Adequate pain control and antibiotic coverage for patients with pack. 2. Avoid Aspirin / NSAIDs 3. Control underlying medical illness 4. If direct pressure is not enough to control bleeding epinephrine-soaked gauze may be placed to bring about vasoconstriction. 5. Cauterisation of bleeding point endoscopically 6. Warm saline irrigation may be tried as a non-invasive measure to control posterior epistaxis 7. Nasal packing – anterior nasal packing, various packing materials are available. (Medicated ribbon gauze or petroleum jelly gauze (0.5 in × 72 in) smeared with an antibiotic ointment is traditionally used. Commercially available Merocel sponge or absorbable materials (e.g. Gelfoam, Surgicel, Avitene) may be used to prevent trauma during packing removal 8. If not controlled posterior nasal packing with inflatable balloon devices 9. A careful endoscopic examination with patient under general anaesthesia may be considered. Bleeding sites may be cauterised, spur or DNS may be

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corrected, and meticulous packing can be done 10. If all the steps fail to control bleeding arterial ligation may be performed - sphenopalatine artery, internal maxillary artery or external carotid artery depending on the case 11. Embolization may be tried in expert centres with facilities. Pre- embolization angiography is performed before procedure 12. Management of hereditary haemorrhagic telangiectasia (HHT) – Options include coagulation with Potassium – Titanyl – Phosphate (KTP) or Neodymium: Yttrium – Aluminium – garnet (Nd: YAG) lasers, septodermoplasty, embolization and oestrogen therapy. Prevention of Epistaxis To the extent possible, patients should avoid the following: ü Strenuous activities - Protection from direct trauma from contact sports activities is afforded using helmets or face pieces. ü Hot and dry environments – The effects of such environments can be mitigated by using humidifiers, better thermostatic control, saline spray, and antibiotic ointment on the Kiesselbach's area. ü Digital trauma – In children, nose picking is difficult to deter. Keeping the child's nails well-trimmed may be helpful. ü Nose blowing and excessive sneezing - Instruct patients to sneeze gently with the mouth open. Inappropriate or careless use of drugs - Consider drug education relating to use or accidental ingestion of aspirin, warfarin (e.g. rat poison in toddlers), or drug abuse in adolescents

72 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section II Flowchart for management of epistaxis is given below

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REFERENCES 1. Moreau S, De Rugy MG, Babin E, Courtheoux P, Valdazo A. Supraselective embolization in intractable epistaxis: review of 45 cases. Laryngoscope. 1998 Jun. 108(6):887-8. 2. Abelson TI. Epistaxis. Schaefer SD. Rhinology and Sinus Disease 1st ed. New York: Mosby; 1998. 43-50. 3. Douglas R, Wormald PJ. Update on epistaxis. Curr Opin Otolaryngol Head Neck Surg. 2007 Jun. 15(3):180-3. 4. Pope LE, Hobbs CG. Epistaxis: an update on current management. Postgrad Med J. 2005 May. 81(955):309-14. 5. Cummings CW. Epistaxis. Cummings. Otolaryngology: Head and Neck Surgery. 4th ed. Philadelphia, Pa: Elsevier, Mosby; 2005. Chap 40. Traboulsi H, Alam E, Hadi U. Changing Trends in the Management of Epistaxis. Int J Otolaryngol. 2015. 2015:263987. 6. Massick D, Tobin EJ. Epistaxis. In: Cummings CW, Haughey BH, Thomas JR, et al, editors. Cummings otolaryngology: head and neck surgery. Philadelphia: Mosby; 2005. p. 942–61. 7. Thornton MA, Mahesh BN, Lang J. Posterior epistaxis: identification of common bleeding sites. Laryngoscope 2005;115(4):588–90. 8. Thomas O. Gifford, MD, Capt. MC, USAF, Richard R. Orlandi, MD, FACS. Otolaryngol Clin N Am 41 (2008) 525–536 9. Schlegel-Wagner C1, Siekmann U, Linder T. Non-invasive treatment of intractable posterior epistaxis with hot-water irrigation; Rhinology. 2006 Mar;44(1):90-3 2.3.ALLERGIC RHINITIS SCOPE This treatment guideline provides clinicians a basis for rational decisions in the management of allergic rhinitis. This guideline is applicable in any setting where patients with allergic rhinitis would be identified, monitored, or managed. It provides guidance for management of typical patients but does not consider all the unique individual circumstances. KEY WORDS Allergic rhinitis, treatment guidelines

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INTRODUCTION Definition Allergic rhinitis is defined clinically by the symptoms caused by immunologically mediated (most often IgE - dependent) inflammation after the exposure of the nasal mucous membranes to offending allergens. Symptoms ü Rhinorrhoea, nasal obstruction or blockage, nasal itching, sneezing, and post-nasal drip that reverse spontaneously or after treatment. Ocular symptoms are also frequent. ü Allergic rhino conjunctivitis is associated with itching and redness of eyes and tearing. ü Other symptoms include itching of palate, post-nasal drip and cough ü Allergic rhinitis is a risk factor for asthma Classification Based on frequency of symptoms: Intermittent – symptoms are present less than 4 days a week or for less than 4 consecutive weeks. Persistent – symptoms are present at least 4 days a week and for at least 4 consecutive weeks. Which are again classified based on Severity (Sleep disturbance, impairment of daily activities, leisure and / or sport, impairment of school or work, troublesome symptom) Mild – none of the above is present Moderate-severe – one or more of the above is present.

Based on temporal pattern of exposure to a triggering allergen Seasonal Perennial Episodic (environmental not normally encountered in patient's environment e.g. visiting a home with pets) Based on these definitions, it is possible that a patient may have intermittent symptoms in perennial allergic rhinitis or persistent symptoms in seasonal allergic rhinitis Diagnosis: ü Characteristic symptoms as mentioned above ü Clinical signs include, but not limited to clear rhinorrhoea, pale mucosa,

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pale to bluish turbinates, red and watery eyes ü External features like allergic shiners, allergic salute, dorsal nasal crease may be present ü Assess for the presence of associated conditions-asthma, atopic dermatitis, sleep disordered breathing, allergic conjunctivitis, sinusitis, OME ü Imaging of paranasal sinuses not required in patients presenting with symptoms consistent with allergic rhinitis. ü Specific IgE (skin and blood) tests may be done in patients who do not respond to empiric treatment, when the diagnosis is uncertain, or when specific causative allergen is to be identified to target therapy Treatment Preventive measures 1. Exclusive breastfeeding for at least 3 months may prevent atopic dermatitis, allergic rhinitis, and asthma 2. Avoidance of allergen- The best and the most desirable when possible. 3. It includes environmental control- removal of pets from indoors, use of air filtration systems (HEPA-High Efficiency Particulate Arresting), impermeable bed covers, use of face masks, Acaricides (Chemical agents that kill dust mites) 4. Avoid exposure to other irritants as cigarette smoke, perfumes, chemicals and exhaust fumes Mild intermittent 1. With nasal congestion - intranasal corticosteroid (ICS) alone or oral anti- histamine with decongestant (phenylephrine or pseudo-ephedrine) or local decongestant for not more than three days 2. Relief with pharmacotherapy- maintain with minimum required dose of ICS 3. If no relief after 2-4weeks - ICS + intranasal anti-histamine (IAH) or ICS + 2nd generation oral anti-histamine (OAH). 4. Consider diagnostic nasal endoscopy/ radiologic evaluation - Turbinate reduction may be done if required 5. With predominant sneezing, itching- II generation OAH / Cromolyn sodium spray (5.2mg/spray 1spray/nose/4-6 times/day or Hydroxy propyl methyl cellulose – 1spray per nostril 2-3 times/day 6. Review after 4weeks- If relief, maintain with minimum dose ICS

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7. No relief in 2-4weeks - consider investigations – Skin prick tests/ID tests and Serum levels of specific Ig by the fluorescence enzyme immunoassay 8. Consider immunotherapy (Sub cutaneous or sublingual) Moderate/severe/persistent symptoms 1. ICS / IAH. If no relief, ICS may be combined with IAH 2. Review after 4weeks- If relief, maintain with minimum dose ICS 3. No relief in 2-4 weeks – A short course of oral steroid may be tried. Step up the dose of INC plus Leukotriene antagonists especially if associated with asthma 4. Consider investigations – Skin prick tests/ID tests and Serum levels of specific Ig by the fluorescence enzyme immunoassay 5. Consider immunotherapy (Sub-cutaneous or sub-lingual) 6. If conjunctivitis is present, add oral antihistamine, intra-ocular H1 antihistamine, intra-ocular cromone 7. If rhinorrhoea is present, add ipratropium nasal spray

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Prophylactics Oral decongestan ts ü Cromolyn spray 5.2mg/spray ü Pseudoephedrine ER 120mg BD Dose:1 spray/nose/4-6 times a day Children ü Pseudoephedrine ER > 12 years ü HPMC powder 4mg/spray ü Pseudoephedrine > 4 years (Hydroxy propyl me thyl cellulose + peppermint - Nezact) Nasal decongestants ü Oxymetazoline not > 3 days Dose:1 spray/nose/2-3 times a day

Leukotriene antagonists ü Montelukast 10mg OD

Children ü Oral antihistamines (II Gen) Monteluk ast > 6 mon th ü Cetirizine 10mg OD ü Lev ocetirizine 5mg OD ü F exofenadine 120mg OD ü Loratadine 10mg OD Intra nasal antihistamines ü ü Desloratadine 5mg OD Azelastine 137 μg/spray > 6 years ü Children Azelastine 206 μg/spray > 6 years ü ü Cetirizine > 6 month Olopatadine 665 μg/spray > 2 years ü ü Azelastine + 137 μg/spray + Desloratadine > 6 mon th ü Fexofenadine > 6 month Fluticasone 50 μg/spray > 12 years ü Loratadine > 2 years Dose 1-2 spray/nose/ once or twice a day (on age)

Anti -cholinergic spray ü Ipratropium bromide 42 µg/spray > 5 years

Dose: 2 sprays/nose three or four times a day

Intra nasal steroids ü Triamcinolone acetonide 55 μg/spr ay > 2 years ü Mome tasone furoate 50 μg/spr ay > 2 years ü Flutic asone furoate 28 μg/spray > 2 years ü Fluticasone propionate 50 μg/ spray > 4 years ü Budesonide (propellant) 32 μg/ spray > 6 years ü Flunisolide (aqueous) 25 μg/spr ay > 6 years ü Ciclesonide (aqueous) 50 μg/spray > 6 years ü Ciclesonide (propellan t) 37 μg/spray > 12 years Pregnancy ü Budesonide (aqueous), Mometasone furoate & Fluticasone propionate Dose 1-2 spray/nose/once or twice a day (on age)

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Flowchart for management of allergic rhinitis is given below

REFERENCES 1. Bozek J L, Agache I et. al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines-2016 revision: J Allergy Clin Immunol. 2017 Oct;140(4):950-958. doi: 10.1016/j.jaci.2017.03.050. Epub 2017 Jun 8 2. Taramarcaz P, Gibson P G. Intranasal corticosteroids for asthma control in people with coexisting asthma and rhinitis. Cochrane database of systemic reviews.2003;3: Cd003570.

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Doi:10.1—2/14651858.CD003570. 3. Bousquet J, Schunemann HJ, Hellings PW, Arnavielhe S, Bachert C, Bedbrook A, et al. MACVIA clinical decision algorithm in adolescents and adults with allergic rhinitis. J Allergy Clin Immunol 2016; 138:367-74. e2. 4. Brozek JL, Baena-Cagnani CE, Bonini S, Canonica GW, Rasi G, van Wijk RG, Zuberbier T, Guyatt G, Bousquet J, Schünemann HJ. Methodology for development of the Allergic Rhinitis and its Impact on Asthma guideline 2008 update. Allergy. 2008 Jan;63(1):38-46. Review 5. AAOHNS Clinical practice guidelines 2015 6. Angelo G. Corsico, MD; Mara De Amici, MSC et.al. Allergy Rhinol (Providence).2017 Mar;8(1): e1- e4.doi:10.2500/ar.2017.8.0187 7. ARIA Guidelines 2016 revision

80 Section III COMMON DISEASES OF THROAT

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Section III 3.1 CUT THROAT INJURY SCOPE Incidence of cut throat injuries and associated morbidity & mortality are not uncommon in present day life. These patients need emergency and multidisciplinary care. Early management can save the life of patients most of the time. INTRODUCTION Cut throat injuries, one of the emergency conditions managed mainly by ENT specialists, pose a great therapeutic challenge because multiple vital organs for phonation, deglutition, vascular and neurological structures vulnerable to injury are present in a small unprotected area. The location of the injury can predict risk and management. Open injuries in the neck inflicted by sharp objects such as razor, knives, or broken bottle pieces or glasses that may be superficial or penetrating in nature may be described as 'cut-throat injuries'4. These may result from accident, homicide, or suicide4. Globally, cut throat injuries account for approximately 5% to 10% of all traumatic injuries with multiple structures being injured in 30% of patients2. According to World Health Organization (WHO), every year over five million people around the world die because of cut throat injury1. In developing countries, the incidence is increasing at a fast rate because of increasing conflict over limited resources, poor socio-economic condition, unemployment, easy access to alcohol and increased crime rate1. These patients need emergency and multidisciplinary care. It has a high mortality rate of 11% and excellent knowledge about the anatomy of the attending physician is mandatory in its management. Zones of neck The neck is commonly divided into three distinct zones, which facilitates initial assessment and management based on the limitations associated with surgical exploration and hemorrhage control unique to each zone. Zone I l Defined inferiorly by the clavicle/sternal notch and superiorly by the horizontal plane passing through the cricoid cartilage.

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l Structures within this zone include the: ü Proximal common carotid arteries. ü Vertebral and subclavian arteries. ü Subclavian, innominate, and jugular veins. ü Trachea. ü Recurrent laryngeal and Vagus nerves. ü Esophagus. ü Thoracic duct. l Vascular structures in this area are in close proximity to the thorax and represent a dangerous area. l Bony thorax, clavicle and sternum protect from injury. l Osseous shield makes surgical access to Zone I difficult and may require sternotomy or thoracotomy to control hemorrhage.

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Zone II l Between the horizontal plane passing through the cricoid cartilage and the horizontal plane passing through the angle of the mandible. l Most frequently involved zone (60% to 75%). l Structures in this zone includes ü Carotid arteries. ü Jugular and vertebral veins, pharynx, and larynx. ü Proximal trachea. ü Recurrent laryngeal and Vagus nerves. ü Spinal cord. l Injuries in this zone are the easiest to expose and evaluate. Zone III l Lies between the horizontal plane passing through the angle of the mandible and the skull base. Anatomic structures within Zone 3 include the: ü Extra-cranial carotid and vertebral arteries. ü Jugular veins. ü Spinal cord. ü Cranial nerves IX–XII. ü Sympathetic trunk. l Because of the cranio-facial skeleton, surgical access to Zone 3 is difficult, making surgical management of vascular injuries challenging with a high associated mortality at the skull base. l Surgical access to Zone III may require craniotomy, as well as mandibulotomy or man oeuvres to anteriorly displace the mandible. l An injury in this area necessitates intra-oral examination for oedema or expanding haematoma within the para-pharyngeal or retro-pharyngeal spaces. In view of the difficult surgical approaches to Zone I and Zone III, all patients with such injuries who are stable and have no evidence of acute airway obstruction, significant bleeding, or expanding haematoma should be evaluated with CT angiography with consideration of barium swallow. Initial management The initial care of patients with penetrating neck injuries should follow the basic tenants of trauma care. The emergent management of all penetrating neck trauma

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requires ü Airway establishment ü Blood perfusion maintenance, and ü Clarification and classification of the severity of the wound In the emergency department, satisfactory control of the airway is established by intubation, cricothyroidotomy, or tracheostomy. l If the trachea is open, insertion of a tracheostomy tube or endotracheal tube through the cut end can be tried after proper suctioning of the airway. This direct transcervical tracheal intubation is safer than oral or nasal intubation when the oral cavity, pharynx, or larynx is traumatized and filled with blood. l In presence of complicated laryngotracheal injury, to avoid further injury to the endolarynx, upfront tracheostomy is appropriate. Large-bore intravenous lines are placed, even when the patient is not hypotensive, so that fluids can be rapidly introduced if necessary. Under no circumstances should a penetrating neck wound be probed because clot dislodgement and uncontrollable bleeding can occur. Arrange blood and inform the operation theatre. Clinical features

Diagnosis Signs and symptoms

l Respiratory distress l Tracheal deviation l Stridor l Subcutaneous Airway injury l Haemoptysis l emphysema l Hoarseness l Sucking wound

l Haematoma l Hypovolemic shock l Persistent bleeding l Bruit Vascular injury l Neurologic deficit l Thrill l Absent pulse l Change of sensorium

l Hemiplegia l Cranial nerve deficit l Quadriplegia l Altered sensorium Nerve injury l Coma l Hoarseness

l Subcutaneous emphysema l Haemoptysis Pharynx / l Dysphagia l Tachycardia oesophagus injury l Odynophagia l Fever l Haematemesis

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Every patient with significant neck trauma should have an X-ray chest and cervical spine done at the earliest. Chest X-ray will help to exclude a haemothorax, pneumothorax, pneumomediastinum (tracheal or oesophageal injury), and widened mediastinum. Cervical spine X-ray is used to exclude spinal column injury and pre-vertebral air (pharyngeal or oesophageal injury). Special investigations such as CT scan, ultrasound and gastrografin or barium studies may only be requested in a haemodynamically stable patient. Definitive management l Obtain brief history regarding the mechanism of injury. l Physical examination should include n Distal carotid and superficial temporal artery pulses. n Peripheral pulses for discrepancy or absence. n Palpation for any thrills and listens for bruits. n Neurologic examination – exclude cranial nerve, brachial plexus and spinal cord injury. n Examination of chest, abdomen and extremities to rule out associated injuries. l Signs of immediate life-threatening injuries warranting immediate mandatory exploration includes ü Massive bleeding ü Rapidly expanding haematoma ü Non-expanding haematoma in the presence of hemodynamic instability ü Hypovolemic shock not responding to resuscitation ü A large blowing wound ü Major haemoptysis ü Haemomediastinum ü Haemothorax Specific injuries Laryngotracheal injury l After securing the airway as mentioned above, the airway injury has to be repaired at the earliest ideally within 24 hours of the injury6. l Significant glottic and supra-glottic lacerations and displaced cartilage fractures need surgical approximation. l If trachea is completely transected, a re-anastomosis of the transected

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ends of the trachea is done. l Sometimes, a segment of the trachea may be badly damaged requiring resection. Here for tension free approximation, laryngeal release or tracheal mobilization may sometimes be needed. l Postoperatively patient's neck is kept flexed for seven to ten days by suturing the chin to the sternum and feeding advocated via nasogastric tube to prevent aspiration. Vascular Injury l The common carotid artery is the most frequently injured major vessel; it accounts for 22% of vascular injuries. Hard clinical signs of vascular injury are expanding haematoma, external haemorrhage, absent or diminished distal pulses, ischaemic neurological deficits, or coma. l The internal jugular vein may be repaired by lateral venorrhaphy, or ligated. If both internal jugular veins have been injured, then at least one vein should be repaired to prevent facial swelling, and sequelae of raised intra-cranial pressure such as blindness, SIADH and even death. l The help of a vascular surgeon is sought for major vessel injury repair. Pharyngeal / oesophageal injury l During neck exploration for a cut throat injury, always evaluate pharynx and esophagus. l Perform manoeuvres to see if there is an injury in pharynx or esophagus (on table endoscopy, air in the nasogastric tube, etc.) and repair it. l If the patient is too unstable for further exploration, do primary diversion of salivary flow to the skin by means of partial or total exteriorization procedures. l Always look for tracheo-oesophageal fistula and if present, repair with interposition of a muscle flap. l Early recognition and treatment is the key to favourable outcome. Missed oesophageal tears represent most of the delayed injuries, and when they progress to mediastinitis, morbidity and mortality are considerable. Chylous injury l Injury to the thoracic duct or right lymphatic duct can cause either chylous leak or chylothorax.

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l Conservative management in the form of medium-chain triglyceride diet and pressure bandage can be attempted, but most often it is uniformly unsuccessful and may necessitates surgical ligation. Neurological injury l Significant brachial plexus nerve injury should be repaired within 24–72 hours. Flow chart on management of cut throat is given below

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REFERENCES 1. Debdulal Chakraborty, Chiranjib Das, Arvind Kumar Verma and Rajesh Hansda. Cut Throat Injury: Our Experience in Rural Set-Up. Indian J Otolaryngology Head Neck Surg. 2017 Mar; 69(1): 35–41. 2. David B. Hom , Robert H. Maisel., Penetrating and Blunt Trauma to the Neck. Cummings otolaryngology– Head and Neck Surgery, 6th edition; pp 1872- 1883. 3. Panchappa SA, Natarajan D, Karuppasamy T, Jeyabalan A, Ramamoorthy RK, Thirani S, Swamirao RK (2014) Cut throat injuries—a retrospective study at a Tertiary Referral Hospital. Int J Otolaryngol Head Neck Surg 3:323–329. 4. Zafarullah Beigh, Rauf Ahmad. Management of cut-throat injuries. The Egyptian Journal of Otolaryngology 2014, 30:268–271. 5. Manilal A, Khorshed ABM, Talukder DC, Sarder RMA, Fakir AT, Hossain M (2011) Cut throat injury: review of 67 cases. Bangladesh J Otorhinolaryngol 17:5–13. 6. Andrew J. Nicol, Johannes J. Fagan. Neck trauma. Scott-Brown's Otorhinolaryngology Head and Neck Surgery, 8th edition pp. 597-605. 7. Roon AJ, Christensen N. Evaluation and treatment of penetrating cervical injuries. J Trauma 1979; 19: 391–7. 8. Gussack GS, Jurkovich GJ, Luterman A. Laryngotracheal trauma: a guidelines approach to a rare injury. Laryngoscope 1986; 96: 660–5. 9. Nathan L. Salinas, Joseph A. Brennan. Penetrating and Blunt Neck Trauma - American Academy of Otolaryngology—Head and Neck Surgery (AAO- HNS). First edition; pp. 164-176. 10. William E. Hurford, Ruben Peralta. Management of tracheal trauma. CAN J ANESTH 2003. 50: 6. pp R1–R6.

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3.2 DYSPHAGIA SCOPE Dysphagia is an important problem faced in daily practice. The problems behind this can range from simple throat infection to conditions that may prove to be fatal. The guidelines outlined here will serve as a blue print in evaluating cases of dysphagia with special emphasis on management of emergency situations. DEFINITION Dysphagia is defined as having difficulty in swallowing which may affect any part of the swallowing pathway from the mouth to stomach1. The approach to which may be medical, surgical, prosthetic or a combination of these depending on the phase of swallowing and age group involved2. INTRODUCTION Dysphagia is a common condition that can have significant impact on the patient quality of life and can be associated with significant complications such as aspiration pneumonia, weight loss and malnutrition. There are three types of dysphagia: oral, oropharyngeal and oesophageal dysphagia. Disorders affecting the oral preparatory and oral propulsive phases cause oral dysphagia. When eating solid food, patients may have difficulty chewing and initiating swallows. When drinking a liquid, patients may find it difficult to contain the liquid in the oral cavity before they swallow. As a result, either liquid drools or spills prematurely into the unprepared pharynx, and this often results in aspiration3 Causes ORAL DYSPHAGIA Table 1 (Page 3-14) OROPHARYNGEAL DYSPHAGIA5 Table 1 (Page 3-14) OESOPHAGEAL DYSPHAGIA5 Table 2 (Page 3-15)

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Table 1: CAUSES OF ORAL DYSPHAGIA

Trismus Disturbance in mastication Fractures of mandible Tumours of upper or lower jaw Disorders of TM joint Disturbance in lubrication Xerostomia Mikulicz disease Paralysis of tongue Disturbance in motility of tongue Painful ulcers Tumours Surgery / Post surgery defects Defects of palate Cleft palate Oronasal fistula Stomatitis Ulcerative lesions Lesions of buccal cavity and floor Ludwig’s angina of mouth Tumours Surgery/Post surgery defects

Table 2: CAUSES OF OROPHARYNGEAL DYSPHAGIA

Structural lesions Examples

Pharyngeal diverticula l Zenker's diverticulum l Lateral pharyngeal pouch or diverticula l Oropharyngeal or laryngeal carcinoma l Surgical resection l Cricopharyngeal achalasia Intrinsic lesions l Cricopharyngeal bar and rings l Proximal oesophageal webs (Plummer-Vinson) l Radiation injury l Osteophytes Extrinsic compression l Skeletal abnormalities l Thyromegaly

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Neuro-musuclar diseases Examples l Cerebro-vascular accident l Head injury l Neoplasm l Parkinson's disease Central nervous system l Multiple sclerosis l Amyotrophic lateral sclerosis l Huntington's chorea

l Poliomyelitis, amyotrophic lateral sclerosis Peripheral nervous l Tabes dorsalis system l Glossitis, pharyngitis, thrush (sensory)

Neuromuscular transmission Myasthenia gravis

l Polymyositis l Dermatomyositis l Muscular dystrophies l Alcoholic myopathy Myopathies l Thyrotoxicosis, Hypothyroidism l Amyloidosis l Cushing's syndrome

Table 3: CAUSES OF OESOPHAGEAL DYSPHAGIA

Neuro-musuclar diseases Examples

l Peptic stricture l Schatzki's ring l Oesophageal carcinoma Intrinsic lesions l Leiomyoma l Lymphoma l Hiatus hernia

l Mediastinal tumours (lung cancer, lymphoma) Extrinsic compression l Vascular structures (dysphagia lusoria) l Surgical changes (fundoplication)

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Motor disorders Examples

l Achalasia l Diffuse oesophageal spasm Primary motor l Hypertensive lower oesophageal sphincter disorders l Nutcracker esophagus l Ineffective oesophageal motility

l Collagen vascular diseases l Scleroderma, Secondary motor l CREST disorders l Diabetes mellitus l Alcoholism Mucosal diseases Examples l Gastrointestinal reflux diseases l Infectious oesophagitis Oesophagitis l Pill-induced l Radiation injury l Caustic ingestion

CARE PATHWAY Assessment of dysphagia Primary care centres Primary care doctors face the challenge of dealing with a heterogeneous group of patients with dysphagia, without immediate access to the diagnostic facilities available in secondary care. As majority of patients with dysphagia will be in fluid deprived sate, access to IV line and other supportive measures can be initiated here along with base line investigations as per the need. Referral criteria Dysphagia due to corrosive poisoning, dysphagia associated with stridor (foreign body obstruction/malignancy) or aspiration should be referred to higher centre immediately Dysphagia cause not diagnosed with the investigation facilities available should also be referred after initiating the necessary primary measures. Secondary care centres As the easily treatable dysphagia will be eliminated at the primary level, secondary care centres face with the difficulty of categorizing dysphagia that

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require emergency surgical intervention (e.g.: dysphagia with airway compromise) or those requiring advanced investigation facilities for identifying the cause. Another category of patients referred here is, cause identified dysphagia for rehabilitation options. As the treatment of dysphagia may be spread over various specialities the referral and admission criteria here will depend on the specialties and the modalities available. Referral criteria Dysphagia requiring emergency surgical intervention where facilities are not available should be referred immediately Dysphagia where rehabilitation facilities are not available should be referred after required investigations. Tertiary care centres Tertiary care centres come face to face with a myriad of patients who are either under or over diagnosed in primary or secondary care centres. They also face with the challenge of prioritizing the cases and triaging to required facilities. History with clinical evaluation 1. Associated symptoms (stridor, aspiration) 2. Preceding factors (corrosive ingestion, foreign body, trauma) 3. Pertaining to age group (congenital, malignancy) 4. General status of the patient (malnutrition, weight loss, dehydration) 5. Medication history 6. ENT and systemic examination Investigations 1. Routine investigations – Complete blood count, ESR, Coagulation profile, Blood sugar, Renal and liver function tests, Serum electrolytes, screening 2. X-ray – soft tissue neck lateral view: obstruction, abscess, foreign body 3. X-ray chest: Aspiration pneumonia 4. Barium swallow (in patients without aspiration) 5. Fibreoptic endoscopic evaluation of swallowing 6. Upper gastrointestinal endoscopy 7. Oesophageal manometry 8. Computed tomography

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9. High resolution intra-luminal ultrasonography. Criteria for admission All cases of absolute dysphagia 1. Dysphagia with malnutrition 2. Dysphagia with airway compromise 3. Dysphagia due to infective causes (e.g. Diphtheria) 4. Corrosive ingestion 5. Dysphagia with foreign body 6. Dysphagia with deep neck space infection

Flowchart for management of dysphagia is given below

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REFERENCES 1. Elfy B Chevretton; Causes of Dysphagia; Scott-Brown's Otorhinolaryngology Head and Neck surgery; 2008; 07:2025 2. Alison Perry; Dysphagia: Management and intervention; Scott-Brown's Otorhinolaryngology, Head and Neck surgery; 2008; 07:2086 3. Lindgren S, Janzon L. Prevalence of swallowing complaints and clinical findings among 50-79-year-old men and women in an urban population. Dysphagia. 1991; 6:187-192. 4. Anita Gasioroeska, Ronnie Fass; Current approach to dysphagia; Gastroenterology and Hepatology; 2009; 5: 269. 5. Jeri A. Logemann, Mechanisms of Normal and Abnormal Swallowing. Cummings Otolaryngology– Head and Neck surgery, 6th edition; pp 1500- 1506. 3.3 DYSPHONIA SCOPE Dysphonia is often caused by benign or self-limited conditions, but it may also be the presenting symptom of a more serious or progressive condition requiring prompt diagnosis and management. These guidelines aim to: ü Define actions that clinicians can take, to deliver quality care. ü Addresses the identification, diagnosis, treatment, and prevention of dysphonia ü Update the needs and management options in special populations and among patients with modifying factors. ü To enhance the accurate diagnosis of dysphonia and its underlying causes, promote appropriate therapeutic options and improve counselling and education for prevention and management of dysphonia. Definition Altered vocal quality, pitch, loudness, or vocal effort that impairs communication as assessed by a clinician and/or affects quality of life1. Hence the management of dysphonia needs to combine both the diagnostic and therapeutic aspects.

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INTRODUCTION Dysphonia (impaired voice production) is a very common complaint affecting nearly one-third of the population at some point in its life. The term dysphonia is often used interchangeably with hoarseness; however, this terminology is imprecise, as hoarseness is a symptom of altered voice quality reported by patients, while dysphonia characterizes impaired voice production as recognized by a clinician. Dysphonia is often caused by benign or self-limited conditions, but it may also be the presenting symptom of a more serious or progressive condition requiring prompt diagnosis and management. Voice disorders affect all ages, but some evidence suggests that risks are higher in paediatric and elderly (>65 years of age) populations. It is important to recognize that patients with head and neck cancer may present with dysphonia. In this group, failure to evaluate the larynx can delay cancer diagnosis. Therefore, the guidelines stands to outline the certain guidelines to ensure prompt diagnosis with minimal yet necessary investigations and proceed with either referral to a higher centre, if at the primary health care level or to decide on a management option. CARE PATHWAY Assessment of dysphonia Primary care centre Most patients (90%) with a complaint of hoarseness initially present to their primary care physicians. Majority of these can be treated effectively at the primary care centre itself, even without immediate access to advanced diagnostic facilities. Clinicians should identify dysphonia in a patient with altered voice quality, pitch, loudness, or vocal effort that impairs communication or reduces quality of life. Referral criteria Dysphonia failing to resolve or improve within 4 weeks or irrespective of duration, or a serious underlying cause is suspected, then refer to a secondary care with facilities to perform laryngoscopy and necessary biopsies to decide on further management.

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Secondary Care: History and examination The history should include, but not be limited to, reviewing ü The duration of the dysphonia ü Type of onset (e.g., sudden, gradual) ü Potential inciting events ü How the condition is affecting the patient ü Associated symptoms (e.g., swallowing, breathing difficulties) ü Current medications, habits (e.g., smoking, alcohol use), ü Concurrent medical conditions and ü Prior surgery ü Careful evaluation allows the clinician to ü Categorize dysphonia severity, ü Develop a treatment plan, and ü Prioritize patients who may need escalated care Physical examination should include a full head and neck examination with attention to listening to the voice (perceptual evaluation). Examination of larynx can be done by indirect mirror laryngoscopy, video-laryngoscopy, video-stroboscopy or flexible laryngoscopy. Neck should be examined for masses, cervical lymphadenopathy or thyroid swelling. Investigations ü Video-laryngoscopy ü Stroboscopy ü Flexible laryngoscopy ü Chest X-ray: to rule out left atrial enlargement (Ortner's syndrome), pulmonary tuberculosis or other granulomatous disease. ü Direct Laryngoscopy and biopsy if indicated. ü Imaging: £ CECT Base of skull to Mediastinum in Unilateral Vocal cord palsy. £ CECT neck; MRI neck only if needed, to ensure early cartilage involvement in malignancy2.

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Criteria for admission ü Most cases do not require admission and can be treated under OP care unless for the following: ü Cases requiring emergency airway management warranting a tracheostomy ü For therapeutic surgical intervention, e.g. MLS ü For diagnostic purpose: biopsy of suspected malignancy. Flow chart on management of dysphonia is given below

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REFERENCES 1. Johns M.M., Sataloff R.T., Merati A.L. et al. Shortfalls of the American Academy of Otolaryngology—Head and Neck Surgery's clinical practice guideline: hoarseness (dysphonia). Otolaryngol Head Neck Surg. 2010; 143:175-180. 2. Jaime I. Chang, Scott E. Bevans,Seth R. Schwartz. Otolaryngology Clinic of North America: Evidence-Based Practice Management of Hoarseness/Dysphonia. Otolaryngol Clin N Am 45 (2012) 1109–1126. 3. Cummings Otolaryngology–Head and Neck Surgery, 6th Edition. page 1587. 4. Mark S. Courey. Injection laryngoplasty. Otolaryngol Clin N Am 37 (2004) 121–138. 5. Lucian Sulica. Laryngoscopy, Stroboscopy and Other Tools for the Evaluation of Voice Disorders. Otolaryngol Clin N Am 46 (2013) 21–30. 3.4 FOREIGN BODY THROAT SCOPE Foreign body throat is a common emergency. This can happen in all age groups and timely and judicious intervention is very important. INTRODUCTION Ingested foreign body is one of the most frequently encountered emergencies in Otolaryngology practice. Many of these foreign bodies get lodged in the upper digestive tract i.e. oropharynx, hypopharynx or oesophagus. Identification and removal of it is very important as they can cause life-threatening suppurative or vascular complications. Most common foreign bodies in children are coins, but marbles, button, batteries, safety pins and bottle tops are also reported. In adults, common foreign bodies are bones, meat bolus, dentures, safety pins and metallic wires. Aetiology 1. Loss of protective mechanism 2. Carelessness: Hasty eating, influence of alcohol 3. Narrowed oesophageal lumen 4. Psychotics

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CARE PATHWAY Primary care centres Primary care doctors face the challenge of dealing with ingested foreign bodies. Since the identification and removal needs proper evaluation and instrumentation, all cases need to be referred appropriately. Secondary care History & Examination: l A proper history is very important in these cases. The nature of foreign body, day of impaction, symptomatology, associated co-morbidities are key points in the identification and further management1. l A proper examination of the oral cavity and oropharynx is to be done. If the foreign body is well visible and proper instruments are available, can be removed. l If the impaction is lower down, a soft tissue X-ray neck lateral view can be advised, and the patient can be referred for appropriate removal. l The absence of radio-opaque shadow in X-ray does not exclude foreign body completely and hence the associated clinical symptoms should be acknowledged and should refer for further management. Referral criteria 1. No facility for endoscopy and impaction of foreign body at hypopharynx or esophagus. 2. Duration of foreign body impaction > 1 day. 3. Nature of foreign body as sharp bones, dentures, safety pins, batteries etc. 4. Site of impaction as hypopharynx, cervical and thoracic esophagus. 5. X-ray negative, but presence of symptoms. 6. Associated with complications as neck space infection, respiratory problems, mediastinitis, perforation etc. 7. Associated with severe co-morbidities. Tertiary care 1. Confirmation of foreign body 2. Endoscopic removal l Most of the foreign bodies in hypopharynx/esophagus can be removed by hypopharyngoscopy / oesophagoscopy under general/ local anaesthesia.

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l Both rigid and flexible scopes have been used to remove foreign bodies from the hypopharynx/esophagus. l Rigid oesophagoscope of appropriate for the size for the patient with proper forceps is preferred. l Soft (meat pieces without bone, vegetable matter) and blunt objects can be removed with flexible scopes. l Special care should be taken in case of a denture especially one with a metal hook pointing upwards. Prompt removal of disc battery is also important as it can lead to complications like stricture, perforation, oesophageal fistula, mediastinitis and death. l 3. CECT Scan Neck +/- Thorax – indications include l Foreign body in X-ray, but failed endoscopy. l No foreign body in X-ray, but patient symptomatic. l Symptomatic patient with duration of foreign body impaction > 1 day l When associated with complications and suspicion of extra-luminal migration. 4. CVTS consultation: Site of impaction in thoracic esophagus and with complications of perforation or mediastinitis. Flow chart on management of foreign

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REFERENCES 1. P.L. Dhingra, Shruti Dhingra, Diseases of Ear, Nose and Throat & Head and Neck Surgery, 6th edition 2014. 2. Divya G.M., Hameed AS, Ramachandran K, Vinayak KV. Extraluminal Migration of Foreign Body: A Report of Two Cases. Int J Head Neck Surg 2013; 4(2):98-101. 3. Al-Sebeih K, Volvoda M, Sobeih A, Al-Sihan M.Perforating and migrating pharyngoesophageal foreign bodies: A series of 5 patients. Ear Nose Throat J. 2006 Sep; 85(9):600-603. 4. Remsen K, Lawson W, Biller HF, Som ML. Unusual presentation of penetrating foreign bodies of upper aerodigestive tract. Ann Otol Rhino Laryngol Suppl.1983;105:32-44. 5. Lue AJ, Fang WD, Manolidis S. Use of plain radiography and computed tomography to identify fish bone foreign bodies. Otolaryngol Head Neck Surg 2000;123(4):435-8. 3.5 DEEP NECK SPACE INFECTIONS SCOPE This guideline is applicable to all medical staff involved in the management of deep neck space infections. It includes general management strategy and detailed management guideliness for the following conditions of peritonsillar abscess, Ludwig's angina, retro-pharyngeal and para-pharyngeal abscess. Definition Deep neck space infection refers to infection in the potential spaces and fascial planes of neck. The management of patients with deep neck space infections comprises early diagnosis and timely intervention to prevent life threatening complications. INTRODUCTION Deep neck space infection remains a common but challenging condition for otorhinolaryngologists and should be treated on emergency basis. The complex anatomy makes diagnosis and precise localization of deep neck infections difficult. Common infections that we encounter include peritonsillar abscess, Ludwig's angina, retro-pharyngeal and para-pharyngeal abscess. Most common primary sources are dental caries, retained foreign body, tonsillitis, infections of salivary

104 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section III glands etc. Usually these infections are poly-microbial in nature. Potentially life- threatening complications have been reported to occur at a rate of 10-20%. Many vital organs are at risk of being involved and the resultant respiratory, vascular, neurologic and systemic complications endanger the life of the patient. Treatment includes broad spectrum antibiotics, airway securing, surgical drainage and eradication of source of infection. Proper diagnosis and prompt management can effectively overcome the disease and provide a cure without complications. CARE PATHWAY Assessment of patient Primary care centre Primary care doctors should be vigilant enough to suspect deep neck space infections in patients presenting with symptoms such as fever, throat pain, dysphagia, dyspnoea with or without neck swelling. Baseline investigations like complete blood count and X-ray can be done here depending on availability. Empiric antibiotic therapy and supportive measures can be initiated here. Referral criteria Patients with breathing difficulty and deteriorating general condition should be referred to higher centre immediately after initiating necessary primary measures. All patients should be referred to higher centre at the earliest if the diagnostic and treatment facilities are not available in primary care centre. Secondary and tertiary care centre ü Proper history and clinical examination give clue about location of inflammatory process as well as its potential severity. Clinical presentation

l Fever, odynophagia, dysphagia, airway compromise - Retro-pharyngeal abscess l Fever, drooling, odynophagia, hot potato voice - Peritonsillar abscess l Fever, swelling below angle of jaw, dysphagia ± dyspnoea -Para-pharyngeal abscess l Fever, pain and swelling sub-mandibular area, odynophagia ± dyspnoea - Ludwig's angina

Aetiological factors

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l Dental caries l Retained foreign body upper aero digestive tract l Upper airway surgery/intubation l Acute rhinosinusitis (paediatric) l Tonsillitis / Pharyngitis l Sialadenitis l Skin cellulitis l IV drug abuse l Infected congenital /acquired cysts l Necrotic malignant lymph nodes

Medical history: Diabetes mellitus/other immune deficiency conditions/drug allergy ü General examination, Head and Neck & Systemic examination ü Investigations Ø Base line blood investigations including Complete blood count, ESR, Coagulation profile, Blood sugar level, Serum electrolytes, Renal function tests and Screening. Ø X- ray soft tissue neck lateral view for evaluation of upper aero- digestive tract and airway compromise. Presence of air fluid level and pre-vertebral widening indicates retro-pharyngeal abscess. Ø X- ray chest PA view to rule out any signs of aspiration or mediastinitis. Ø Ultrasonography of neck is helpful in cases of Ludwig's angina and para-pharyngeal space involvement, but it has a limited role in deep spaces like retro-pharyngeal space involvement. Ø CECT Neck provides information about the neck spaces involved, their extent and complications. Ø Pus culture and sensitivity if possible. ü Dental (caries teeth), paediatric surgery (acute retro-pharyngeal abscess in children) and CVTS (mediastinal involvement) consultations if needed.

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Treatment 1. All patients should be admitted. 2. Airway complication should be anticipated in all cases. 3. Initial management of any patient with known or suspected deep neck space infection is securing the airway. This can be done either by intubation or tracheostomy. In retro-pharyngeal abscess, if intubation is attempted, it should be done carefully by an experienced anaesthesiologist and all care should be taken to prevent accidental rupture. 4. IV access should be obtained and give supportive care, broad spectrum antibiotics and analgesics. Steroids can be given, if clinically indicated. 5. Then proceed with surgical drainage of the abscess depending on the spaces involved and do tracheostomy if needed. 6. Primary source of infection should be eradicated. 7. “If patient is clinically stable and otherwise healthy with abscess cavities less than 2.5cm in diameter and involving a single neck space, a 48 – 72 hour trial of empiric IV antibiotic therapy is appropriate”1

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Flowcharts on management of various abscesses are given below

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REFERENCES 1. James M. Christian, Adam C. Goddard, M. Boyd Gillespie. Deep Neck and Odontogenic Infections. Cummings Otolaryngology Head and Neck Surgery, 6th edition pp. 164-175. 2. James W. Moor. Neck space infections. Scott-Brown's Otorhinolaryngology Head and Neck Surgery, 8th edition pp. 623-632. 3. Gujrathi A.B., Ambulgekar V, Kathait P. Deep neck space infection – A retrospective study of 270 cases at tertiary care center. World Journal of Otorhinolaryngology - Head and Neck Surgery. 2016; 2(4):208-213. 4. Motahari S.J., Poormoosa R., Nikkhah M., Bahari M., Shirazy S.M.H., Khavarinejad F. Treatment and Prognosis of Deep Neck Infections. Indian Journal of Otolaryngology and Head & Neck Surgery. 2015; 67 (Suppl 1):134- 137. 5. Francisco Vieira, Shawn M. Allen, Rose Mary S. Stocks, Jerome W. Thompson. Deep Neck Infection. Otolaryngol Clin N Am 41 (2008) 459–483.

3.6 STRIDOR SCOPE This guideline is applicable to all medical staff involved in management of stridor. This guideline will act as a reference in the hospitals and primary care centres and it includes the general management strategy, detailed management guidelines for stridor and the general guidelines on the primary care or ambulatory care of stridor. INTRODUCTION Stridor is noisy respiration produced by turbulent airflow through narrowed air passages. It may be heard during inspiration, expiration or both. l Inspiratory: obstruction at and above the glottic larynx. l Expiratory: obstruction of the intra-thoracic airway. l Biphasic: obstruction associated with sub-glottic and tracheal lesions.

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STRIDOR ACQUIRED ETIOLOGY CONGENITAL

ü Laryngomalacia AFEBRILE FEBRILE ü Laryngeal web ü Papillomatosis ü Epiglottitis ü Sub-glottic stenosis ü Injury ü Acute laryngitis ü Hemangioma ü Foreign body ü Laryngotracheitis ü VC palsy ü Laryngeal oedema ü Diphtheria ü T ongue & jaw ü Malignancy ü RP abscess abnormalities ü IMN

ü Peritonsillar abscess

CARE PATHWAY Primary care centres Primary care doctors face the challenge of dealing with stridor from any causes listed above due to unavailability of facilities to secure airway. Hence all cases are to be referred Secondary care History & Examination

First, confirm the noisy breathing is stridor and record vitals including SpO2.

Secure an IV line and start O2 inhalation. Intravenous steroids should be given along with nebulization with steroids. Meanwhile a proper brief history should be taken to identify the cause of stridor and should include the following: 1. Onset & duration 2. Similar episodes in the past 3. Foreign body ingestion / Anaphylaxis 4. Under influence of alcohol/cannabis/sedatives 5. Associated symptoms – hoarseness, dysphagia 6. History of COPD 7. History of surgery/intubation/trauma 8. Treatment history in the form of radiation /chemotherapy. A quick examination to be done to assess the neck, chest and airway. Look for swellings, dilated veins & scars over neck. Assess the laryngeal frame

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work, look for widening & CVC. If stable, perform an indirect laryngoscopy examination to assess the glottic space. Auscultate chest to look for any adventitious sounds. If patient improves, continue close monitoring of vitals & supportive management. If not improving, plan to secure airway according to level of obstruction. Referral criteria If facilities for intubation or tracheostomy is not available, patient should be referred immediately. Tertiary care In addition to the initial measures listed above, X-ray Soft tissue neck lateral view may be taken. The cause of stridor should be identified and managed by airway intubation or tracheostomy.

Flow chart of management of stridor is given below

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REFERENCES 1. Paul Pracy, Peter Conboy. Upper airway obstruction and tracheostomy. Scott-Brown's Otorhinolaryngology Head and Neck Surgery, 8th edition pp. 1037-1048. 2. Shannon M. Kraft, Joshua S. Schindler. Tracheotomy. Cummings Otolaryngology Head and Neck Surgery, 6th edition pp. 95-103. 3. P.L. Dhingra, Shruti Dhingra, Diseases of Ear, Nose and Throat & Head and Neck Surgery, 6th edition 2014. 4. Benjamin D. Liess, Troy D. Scheidt, Jerry W. Templer. The Difficult Airway. Otolaryngol Clin N Am 41 (2008) 567–580. 5. Claudia Russell, Basil Matta. Tracheostomy- a multi-professional hand

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Section IV ENT EMERGENCIES

STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section IV

Section IV 4.1 FACIAL TRAUMA SCOPE Include general and detailed strategy for management of facial trauma. AIM To develop guidelines for management of patients with facial trauma. INTRODUCTION Faciomaxillary injuries are very common in RTA. It can cause bony as well as soft tissue injuries. Injuries have a potential to interfere with airway, cause disfigurement and loss of function. Hence proper evaluation and early intervention is a must. CARE PATHWAY Primary care center Airway should be assessed and secured if possible before referring the patient. Visual deficits should be ruled out. Minor injuries including contusions, abrasions, lacerations, incised wounds may be managed at PHC. Referral criteria ü Compromised airway ü Visual compromise ü Suspected fracture of facial bones ü Uncontrolled epistaxis ü Extensive soft tissue injuries Investigations ü CBC, Coagulation profile ü CT Brain / PNS

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SectionST IV Flowchart for management of vertigo is given below ANDARD TREA TMENT GUIDELINES ON COMMONEARDISEASES

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4.2 EAR TRAUMA SCOPE Incudes general and detailed management strategy for patients with ear trauma, complaining of ear bleed, facial palsy, pinna injury, hard of hearing or vertigo. AIM To develop criteria for management of patients attending emergency medicine department with ear trauma regarding admission / conservative / surgical management INTRODUCTION Ear trauma can be blunt or penetrating, the impact of which can vary from pinna laceration, traumatic tympanic membrane perforation, facial nerve palsy, fracture temporal bone, labyrinthine concussion, hearing loss and ear bleed. Prognosis largely depends on the accurate diagnosis and timely intervention. Ear trauma is usually associated with other injuries including traumatic brain injury, abdominal trauma and other orthopedic injuries. In this scenario, there is high chance of ear trauma going unnoticed, resulting in permanent handicap. CARE PATHWAY Primary Health center Isolated ear trauma including lacerated pinna injury/traumatic perforation can be managed at PHC Referral criteria ü Mutilated pinna ü Amputated pinna ü Facial palsy ü Vertigo and ear bleed, if HRCT facility is not available ü Lack of availability of ENT specialist MANAGEMENT OF EAR TRAUMA ü Asses the general condition ü ABC to be established ü Detailed history and proper ENT examination ü Investigations ü CBC, URE, Coagulation profile ü CT brain

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ü Special investigations include HRCT Temporal bone and PTA

ü Criteria for admission ü All trauma cases with ü Vertigo ü Facial Paralysis ü Mutilated / amputated / hematoma pinna ü SNHL Flowchart for management of ear trauma is given below

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4.3 FACIAL PARALYSIS SCOPE Includes general and detailed management strategy for facial paralysis AIM To develop criteria for management of patients attending emergency medicine department with facial paralysis INTRODUCTION Facial paralysis can occur isolated or along with CVA. Isolated facial paralysis will be managed in ENT. Post traumatic palsy needs detailed evaluation to decide regarding surgical intervention. CARE PATHWAY Primary care center Detailed history and examination to be done. If idiopathic, it can be managed at primary care center conservatively. Referral criteria ü Post traumatic ü Associated hearing loss ü Vesicles around the ear ü Other neurological deficits ü If associated COM/MOE/AOM Investigations ü RBEURE ü CT Brain HRCT Temporal bone ü Pure tone Audiogram ü Criteria for Admission ü Associated with complications (AOM & COM) ü MOE ü Post traumatic

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SectionST IV Flowchart on management of facial paralysis is given below ANDARD TREA TMENT GUIDELINES ON COMMONEARDISEASES

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4.4 EAR ACHE SCOPE Includes general management strategy and detailed guidelines for ear ache which is associated with ear discharge, hard of hearing, itching ear, and referred otalgia. AIM To develop criteria for management of patients attending emergency department with earache regarding diagnosis and management. INTRODUCTION Otalgia can be primary or referred. Typical causes of primary otalgia include otitis externa, otitis media, mastoiditis and auricular infections. Many remote anatomic sites share common innervation of ear and pathologies in these areas may be perceived as otalgia. Definition Otalgia or earache has two distinct types, pain that originates within the ear is primary otalgia & pain that originates outside the ear is referred otalgia. CARE PATHWAY Primary health center ü Otitis externa and media without complications can be managed at PHC. ü Oral causes should be treated accordingly. Referral criteria ü Suspicion of complications in AOM / COM / Malignant otitis externa ü Suspicion of malignancy of upper aerodigestive tract Investigations ü CBC, RFT, LFT, RBS, HRCT Temporal bone, PTA

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SectionST IV

Flowchart on management of earache is given below ANDARD TREA TMENT GUIDELINES ON COMMONEARDISEASES

STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section IV

4.5 FOREIGN BODY EAR SCOPE Includes general and specific management of foreign bodies in the ear, which is common in the pediatric population INTRODUCTION Foreign body ear is common in children and adults. It may even be an incidental finding. They can be live or inanimate. Proper examination should be done to identify the foreign body and removal done with least trauma possible. Corrosive foreign bodies (e.g. Button batteries) are best removed as early as possible. Long forgotten corrosive foreign bodies may cause extensive erosion and granulations; their removal is fraught with danger and done better by experts. CAREPATHWAY Primary health center Removal may be attempted at primary care centers if the following criteria is met ü FB is visible, non-impacted ü No history of ear discharge/ tympanic membrane is intact Can be attempted by instrumentation / Syringing (to be avoided in vegetable / hygroscopic foreign bodies Referral criteria ü Impacted FB ü Suspected FB in middle ear ü Facial Nerve Palsy ü Previously attempted and failed removal Investigations ü Examination under microscope ü HRCT temporal bone if complications like Facial palsy/ ossicular disruption TREATMENT 1. If live foreign body like insect, kill it with liquid paraffin or sterile water before removal 2. If visible, and not impacted, removal in emergency with grasping forceps, wax hook or micro suction. If tympanic membrane is intact and foreign body is non-vegetable, syringing can be tried. Do not syringe if tympanic

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membrane is perforated. 3. If not visible, removal under GA in children and non-cooperative adults. 4. Use surgical microscope in impacted / complicated FB. 5. Post aural approach if needed for impacted FB.

Flowchart on management of foreign body ear is given below

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4.6 FOREIGN BODY NOSE SCOPE Includes general and specific management of foreign bodies in the nose, which is common in the pediatric population INTRODUCTION Foreign body nose is common in children and mentally retarded adults. It should be suspected in any child with unilateral nasal discharge. Proper examination should be done to identify the foreign body and for timely removal. CAREPATHWAY Primary health center Removal may be attempted at primary care centers if FB is visible. Referral criteria ü Posteriorly located FB ü Suspected FB if not visualized ü Rhinolith ü Previously attempted and failed removal Investigations ü X-ray PNS if radio-opaque FB is suspected and not visualized on examination ü Diagnostic nasal endoscopy ü CT PNS TREATMENT 1. If visible, removal in emergency followed by decongestants and antibiotics. 2. If not visible, endoscopic removal under GA in children and mentally retarded adults. Endoscopic / external approach in case of rhinolith.

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Flowchart on management of foreign body nose is given below

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4.7 HEADACHE SCOPE This guideline is to define the management criteria for all patients with headache coming to ENT department. AIM To develop a guidelines for medical & surgical management of headache and to define referral criteria. INTRODUCTION Headache is one of the most common symptoms presenting in ENT casualty. It can occur due to variety of causes. Depending upon the cause, it can be managed at a primary care center or referred to higher center. Primary care center Any uncomplicated sinusitis, headache due to viral illness or headache with typical auras of migraine can be managed at primary care center. Referral criteria Any clinical suspicion of complication in sinusitis or headache not responding to conventional treatment can be referred to secondary or tertiary care center where expert ENT surgeon, neurosurgeon and investigation facilities are available. Aetiology Sinusitis ü If patients had viral rhinitis, there is high chance for developing secondary sinusitis ü Recent facial trauma ü Caries teeth ü Gross deviation of nasal septum which is obstructing the ostiomeatal complex. Complications of sinusitis ü Associated fever and constitutional symptoms – possibility of viral illness. ü Purulent nasal or post nasal discharge – sinusitis. Acute sinusitis – pain & tenderness over the sinus. Chronic sinusitis– only heaviness of head. Non-invasive fungal sinusitis also can present with headache. ü Orbital complications presenting with proptosis, chemosis, diminished

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vision in one eye – orbital cellulitis ü If both eyes involved – cavernous sinus thrombosis ü Associated nerve involvement–superior orbital fissure syndrome or orbital apex syndrome. ü Osteomyelitis of sinuses ü Neck rigidity – Meningitis ü Co-existent diabetes or other immune-compromised states –invasive fungal sinusitis like mucormycosis and aspergillosis. Space occupying lesions of brain ü Headache + localizing signs + projectile vomiting – intracranial space occupying lesions. Neurovascular headache ü Migraine: Typical auras with unilateral headache, diplopia, intolerance to sound and light, nausea, vomiting followed by remission. Family history/similar episodes earlier may be there. ü Trigeminal neuralgia ü Cluster headache ü Herpes zoster Investigations ü Digital X-ray PNS-sinusitis ü CT scan head - if suspicion of intracranial lesions ü CT scan orbit nose and PNS – if suspicion of orbital cellulitis ü MRI brain – cavernous sinus thrombosis, meningitis ü Diagnosis of vascular headache is purely based on clinical examination and by excluding other causes. Treatment 1. Acute Bacterial Sinusitis Broad spectrum antibiotics like Co- amoxiclav 625 mg TDS for 10 - 14 days. In penicillin sensitive patients, Erythromycin 500mg QID can be tried. Analgesics like paracetamol and antihistamines like chlorpheniramine maleate given if associated with nasal allergy. Surgery – FESS in non- responding cases. 2. Fungal Sinusitis Non-invasive cases: FESS + steroid sprays Invasive cases: ESS debridement + antifungal treatment. IV Amphotericin

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for mucormycosis. 3. Complications of sinusitis Orbital cellulitis: Parenteral antibiotics + immediate orbital decompression after having ophthalmology consultation. Cavernous sinus thrombosis: Neurology reference. FESS for primary pathology. Meningitis: Neurology reference Brain abscess: Neurosurgery reference 4. Migraine Flunarizine 10 mg HS or Propranolol 40 mg BD can be tried for long periods. Neurology reference for resistant cases and other vascular headaches

Flow chart for headache is given below

133 STANDARD TREATMENT GUIDELINES ON COMMON EAR DISEASES Section IV

4.8 VERTIGO SCOPE Includes general and detailed management strategy for vertigo AIM To develop criteria for management of patients with vertigo attending emergency medicine department INTRODUCTION Vertigo may be caused due to central or peripheral pathologies. Identification of the cause is very important for the proper management. Peripheral vertigo is managed in ENT. Common causes of peripheral vertigo include BPPV, Meniere's disease, vestibular neuronitis, labyrinthitis. CARE PATHWAY Primary health center Detailed history and evaluation should be done to differentiate central and peripheral types. Central vertigo should be referred to a higher center for detailed evaluation. Position test and Epley manoeuvre can be tried by trained doctors. For other cause vestibular sedatives may be administered before referring to higher centers. Referral criteria ü Vertigo associated with other neurological deficits ü Suspected complication of COM ü Intractable vertigo ü Associated with hearing loss or tinnitus Investigations ü CBC, RFT, LFT, RBS ü X-ray Cervical spine ü PTA ü Caloric test if indicated ü HRCT Temporal bone / CT brain in selected cases ü HINTS plus test is used to differentiate central and peripheral causes. It includes Head Impulse test, Nystagmus, Test of Skew Deviation (vertical) and hearing test (finger rub test which is the + component)

134 Flowchart for management of vertigo is given below ST ANDARD TREA TMENT GUIDELINES ON COMMONEARDISEASES

Section IV 135

Department Of Health And Family Welfare Government Of Kerala Annexe II, Secretariat Thiruvananthapuram

Kerala-695001 February 2021 Kerala HEALTH